Faculty Profiles - NAKATSUKA Atsuko

写真a

NAKATSUKA Atsuko

Organization

Scheduled update Lecturer

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Degree

医学博士 ( 岡山大学 )

Research Interests

糖尿病
肥満症
腎臓病
脂質異常症

Research Areas

Life Science / Metabolism and endocrinology
Life Science / Nephrology

Education

Okayama University 医学部医学科

1992.4 - 1998.3

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Research History

Okayama University 腎臓・糖尿病・内分泌内科 Lecturer

2019.7

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Okayama University 腎臓・糖尿病・内分泌内科 Assistant Professor

2014.4 - 2019.6

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Okayama University Graduate School of Medicine , Dentistry and Pharmaceutical Sciences Assistant Professor

2012.7 - 2014.3

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Professional Memberships

日本動脈硬化学会

2021.7
JAPAN SOCIETY FOR THE STUDY OF OBESITY

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JAPANESE SOCIETY OF NEPHROLOGY

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Japanese Society for Treatment of Obesity

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Japanese Society for Dialysis Therapy

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The Japan Endocrine Society

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American College of Physicians

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糖尿病合併症学会

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THE JAPAN DIABETES SOCIETY

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THE JAPANESE SOCIETY OF INTERNAL MEDICINE

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Committee Memberships

日本肥満学会学術委員会委員

2024.4

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日本肥満学会教育委員会委員

2024.4

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日本肥満学会専門医カリキュラム委員会委員

2024.4

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日本肥満学会総務委員会委員

2024.4

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日本肥満学会専門医カリキュラム委員会委員

2021.1

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Committee type：Academic society

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日本腎臓学会腎臓学会　症例評価委員

2021.1 - 2022.3
日本腎臓学会 CKD診療ガイドライン改訂委員会作成委員

2020.8

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日本肥満学会肥満症専門医認定試験委員

2020.5

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Committee type：Academic society

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日本肥満学会専門医認定試験委員

2020.5 - 2021.12

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Committee type：Academic society
日本肥満学会教育委員会委員

2020.5 - 2021.12
日本腎臓学会評議員

2020.4

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日本腎臓学会 JSN Next Frontier 2028委員会

2020.4

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Committee type：Academic society

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日本肥満学会評議員

2019.11

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Committee type：Academic society

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日本糖尿病学会中国・四国支部評議員

2019.5

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Committee type：Academic society

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日本内科学会中国支部評議員

2013.6

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Committee type：Academic society

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JSN Next Frontier 2028委員会

2000.9 - 2022.3

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Papers

GRP78 Contributes to the Beneficial Effects of SGLT2 Inhibitor on Proximal Tubular Cells in DKD Reviewed

Atsuko Nakatsuka, Satoshi Yamaguchi, Jun Wada

Diabetes 73 ( 5 ) 763 - 779 2024.2

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Authorship：Lead author,　Corresponding author Language：English Publishing type：Research paper (scientific journal) Publisher：American Diabetes Association

The beneficial effects of sodium–glucose cotransporter 2 (SGLT2) inhibitors on kidney function are well-known; however, their molecular mechanisms are not fully understood. We focused on 78-kDa glucose-regulated protein (GRP78) and its interaction with SGLT2 and integrin-β1 beyond the chaperone property of GRP78. In streptozotocin (STZ)-induced diabetic mouse kidneys, GRP78, SGLT2, and integrin-β1 increased in the plasma membrane fraction, while they were suppressed by canagliflozin. The altered subcellular localization of GRP78/integrin-β1 in STZ mice promoted epithelial mesenchymal transition (EMT) and fibrosis, which were mitigated by canagliflozin. High-glucose conditions reduced intracellular GRP78, increased its secretion, and caused EMT-like changes in cultured HK2 cells, which were again inhibited by canagliflozin. Urinary GRP78 increased in STZ mice, and in vitro experiments with recombinant GRP78 suggested that inflammation spread to surrounding tubular cells and that canagliflozin reversed this effect. Under normal glucose culture, canagliflozin maintained sarco/endoplasmic reticulum (ER) Ca2+-ATPase (SERCA) activity, promoted ER robustness, reduced ER stress response impairment, and protected proximal tubular cells. In conclusion, canagliflozin restored subcellular localization of GRP78, SGLT2, and integrin-β1 and inhibited EMT and fibrosis in DKD. In nondiabetic chronic kidney disease, canagliflozin promoted ER robustness by maintaining SERCA activity and preventing ER stress response failure, and it contributed to tubular protection.

Article Highlights

DOI： 10.2337/db23-0581

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A Vaspin–HSPA1L complex protects proximal tubular cells from organelle stress in diabetic kidney disease Reviewed International journal

Atsuko Nakatsuka, Satoshi Yamaguchi, Jun Eguchi, Shigeru Kakuta, Yoichiro Iwakura, Hitoshi Sugiyama, Jun Wada

Communications Biology 4 ( 1 ) 373 - 373 2021.12

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Authorship：Lead author,　Corresponding author Language：English Publishing type：Research paper (scientific journal) Publisher：Springer Science and Business Media LLC

<title>Abstract</title>Proximal tubular cells (PTCs) are crucial for maintaining renal homeostasis, and tubular injuries contribute to progression of diabetic kidney disease (DKD). However, the roles of visceral adipose tissue-derived serine protease inhibitor (vaspin) in the development of DKD is not known. We found vaspin maintains PTCs through ameliorating ER stress, autophagy impairment, and lysosome dysfunction in DKD. <italic>Vaspin</italic>−/− obese mice showed enlarged and leaky lysosomes in PTCs associated with increased apoptosis, and these abnormalities were also observed in the patients with DKD. During internalization into PTCs, vaspin formed a complex with heat shock protein family A (Hsp70) member 1 like (HSPA1L) as well as 78 kDa glucose-regulated protein (GRP78). Both vaspin-partners bind to clathrin heavy chain and involve in the endocytosis. Notably, albumin-overload enhanced extracellular release of HSPA1L and overexpression of HSPA1L dissolved organelle stresses, especially autophagy impairment. Thus, vapsin/HSPA1L-mediated pathways play critical roles in maintaining organellar function of PTCs in DKD.

DOI： 10.1038/s42003-021-01902-y

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Other Link： http://www.nature.com/articles/s42003-021-01902-y
Plasma angiotensin-converting enzyme 2 (ACE2) is a marker for renal outcome of diabetic kidney disease (DKD) (U-CARE study 3). Reviewed International journal

Asami Ueno, Yasuhiro Onishi, Koki Mise, Satoshi Yamaguchi, Ayaka Kanno, Ichiro Nojima, Chigusa Higuchi, Haruhito A Uchida, Kenichi Shikata, Satoshi Miyamoto, Atsuko Nakatsuka, Jun Eguchi, Kazuyuki Hida, Akihiro Katayama, Mayu Watanabe, Tatsuaki Nakato, Atsuhito Tone, Sanae Teshigawara, Takashi Matsuoka, Shinji Kamei, Kazutoshi Murakami, Ikki Shimizu, Katsuhito Miyashita, Shinichiro Ando, Tomokazu Nunoue, Jun Wada

BMJ open diabetes research & care 12 ( 3 ) 2024.5

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INTRODUCTION: ACE cleaves angiotensin I (Ang I) to angiotensin II (Ang II) inducing vasoconstriction via Ang II type 1 (AT1) receptor, while ACE2 cleaves Ang II to Ang (1-7) causing vasodilatation by acting on the Mas receptor. In diabetic kidney disease (DKD), it is still unclear whether plasma or urine ACE2 levels predict renal outcomes or not. RESEARCH DESIGN AND METHODS: Among 777 participants with diabetes enrolled in the Urinary biomarker for Continuous And Rapid progression of diabetic nEphropathy study, the 296 patients followed up for 9 years were investigated. Plasma and urinary ACE2 levels were measured by the ELISA. The primary end point was a composite of a decrease of estimated glomerular filtration rate (eGFR) by at least 30% from baseline or initiation of hemodialysis or peritoneal dialysis. The secondary end points were a 30% increase or a 30% decrease in albumin-to-creatinine ratio from baseline to 1 year. RESULTS: The cumulative incidence of the renal composite outcome was significantly higher in group 1 with lowest tertile of plasma ACE2 (p=0.040). Group 2 with middle and highest tertile was associated with better renal outcomes in the crude Cox regression model adjusted by age and sex (HR 0.56, 95% CI 0.31 to 0.99, p=0.047). Plasma ACE2 levels demonstrated a significant association with 30% decrease in ACR (OR 1.46, 95% CI 1.044 to 2.035, p=0.027) after adjusting for age, sex, systolic blood pressure, hemoglobin A1c, and eGFR. CONCLUSIONS: Higher baseline plasma ACE2 levels in DKD were protective for development and progression of albuminuria and associated with fewer renal end points, suggesting plasma ACE2 may be used as a prognosis marker of DKD. TRIAL REGISTRATION NUMBER: UMIN000011525.

DOI： 10.1136/bmjdrc-2024-004237

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Inhibition of Amino Acids Influx into Proximal Tubular Cells Improves Lysosome Function in Diabetes. Reviewed International journal

Yuzuki Kano, Satoshi Yamaguchi, Koki Mise, Chieko Kawakita, Yasuhiro Onishi, Naoko Kurooka, Ryosuke Sugawara, Haya Hamed Hassan Albuayjan, Atsuko Nakatsuka, Jun Eguchi, Jun Wada

Kidney360 2023.12

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BACKGROUND: Inhibition of glucose influx into proximal tubular cells (PTCs) by sodium-glucose co-transporter 2 (SGLT2) inhibitors revealed prominent therapeutic impacts on diabetic kidney disease (DKD). Collectrin (CLTRN) serves as a chaperone for the trafficking of neutral amino acid transporters in the apical membranes of proximal tubular cells. We investigated the beneficial effects of reduced influx of amino acids into proximal tubular cells in diabetes and obesity model of Cltrn-/y mice. METHODS: Cltrn+/y and Cltrn-/y mice at 5 weeks of age were assigned to standard diet- (STD) and streptozotocin and high fat diet-treated (STZ-HFD) groups. RESULTS: At 22-23 weeks of age, body weight and HbA1c levels significantly increased in STZ-HFD-Cltrn+/y compared to STD-Cltrn+/y; however, they were not altered in STZ-HFD-Cltrn-/y compared to STZ-HFD-Cltrn+/y. At 20 weeks of age, urinary albumin creatinine ratio (UACR) was significantly reduced in STZ-HFD-Cltrn-/y compared to STZ-HFD-Cltrn+/y. Under the treatments with STZ and HFD, the Cltrn gene deficiency caused significant increase in urinary concentration of amino acids such as Gln, His, Gly, Thr, Tyr, Val, Trp, Phe, Ile, Leu and Pro. In proximal tubular cells in STZ-HFD-Cltrn+/y, the enlarged lysosomes with diameter of 10 μm or more were associated with reduced autolysosomes, and the formation of giant lysosomes was prominently suppressed in STZ-HFD-Cltrn-/y. Phospho-mTOR and inactive form of phospho-TFEB were reduced in STZ-HFD-Cltrn-/y compared to STZ-HFD-Cltrn+/y. CONCLUSIONS: The reduction of amino acids influx into proximal tubular cells inactivated mTOR, activated TFEB, improved lysosome function, and ameliorated vacuolar formation of PTCs in STZ-HFD-Cltrn-/y mice.

DOI： 10.34067/KID.0000000000000333

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Circulating GPIHBP1 levels and microvascular complications in patients with type 2 diabetes: A cross-sectional study. Reviewed International journal

Naoko Kurooka, Jun Eguchi, Kazutoshi Murakami, Shinji Kamei, Toru Kikutsuji, Sakiko Sasaki, Akiho Seki, Satoshi Yamaguchi, Ichiro Nojima, Mayu Watanabe, Chigusa Higuchi, Akihiro Katayama, Haruhito A Uchida, Atsuko Nakatsuka, Kenichi Shikata, Jun Wada

Journal of clinical lipidology 16 ( 2 ) 237 - 245 2022.1

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BACKGROUND: Glycosylphosphatidylinositol-anchored high-density lipoprotein binding protein 1 (GPIHBP1) plays a crucial role in lipolytic processing. Previous studies have shown that GPIHBP1 mutations cause severe hypertriglyceridemia and that serum GPIHBP1 levels are marginally higher in patients with coronary heart disease; however, the role of GPIHBP1 in type 2 diabetes mellitus (T2DM) remains unknown. OBJECTIVE: We investigated the association between circulating GPIHBP1 levels and the prevalence of microvascular complications in T2DM. METHODS: A total of 237 subjects with T2DM and 235 non-diabetic control subjects were enrolled in this study. Their serum GPIHBP1 levels were evaluated using ELISA assays. RESULTS: Circulating GPIHBP1 levels were higher in patients with T2DM (952.7 pg/mL [761.3-1234.6], p < 0.0001) than in non-diabetic subjects (700.6 [570.8-829.6]), but did not differ in T2DM patients with or without hypertriglyceridemia. Serum GPIHBP1 levels were significantly higher in patients with T2DM with diabetic retinopathy (DR), diabetic nephropathy (DN), and microvascular complications than in those without these complications. Multivariable logistic regression and receiver operating characteristic (ROC) curve analyses revealed that the presence of microvascular complications, but not macrovascular complications, was independently associated with serum GPIHBP1 levels, which could predict the presence of diabetic microvascular complications. CONCLUSIONS: Elevated GPIHBP1 levels are associated with microvascular complications in T2DM and may help to predict their progression.

DOI： 10.1016/j.jacl.2022.01.006

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Author Correction: Lgals9 deficiency ameliorates obesity by modulating redox state of PRDX2 (Scientific Reports, (2021), 11, 1, (5991), 10.1038/s41598-021-85080-1) Reviewed

Tomokazu Nunoue, Satoshi Yamaguchi, Sanae Teshigawara, Akihiro Katayama, Atsuko Nakatsuka, Jun Eguchi, Toshiro Niki, Jun Wada

Scientific Reports 11 ( 1 ) 2021.12

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Language：English Publishing type：Research paper (scientific journal) Publisher：Nature Research

DOI： 10.1038/s41598-021-98293-1

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Lgals9 deficiency ameliorates obesity by modulating redox state of PRDX2 Reviewed International journal

Tomokazu Nunoue, Satoshi Yamaguchi, Sanae Teshigawara, Akihiro Katayama, Atsuko Nakatsuka, Jun Eguchi, Toshiro Niki, Jun Wada

Scientific Reports 11 ( 1 ) 5991 - 5991 2021.12

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Language：English Publishing type：Research paper (scientific journal) Publisher：Springer Science and Business Media LLC

<title>Abstract</title>The adipose tissue is regarded as an endocrine organ and secretes bioactive adipokines modulating chronic inflammation and oxidative stress in obesity. Gal-9 is secreted out upon cell injuries, interacts with T-cell immunoglobulin-3 (Tim-3) and induces apoptosis in activated Th1 cells. Gal-9 also binds to protein disulfide isomerase (PDI), maintains PDI on surface of T cells, and increases free thiols in the disulfide/thiol cycles. To explore the molecular mechanism of obesity, we investigated Gal-9^−/− and Gal-9^wt/wt C57BL/6J mice fed with high fat-high sucrose (HFHS) chow. Gal-9^−/− mice were resistant to diet-induced obesity associated with reduction of epididymal and mesenteric fat tissues and improved glucose tolerance compared with Gal-9^wt/wt mice. However, the number of M1, M2 macrophages, and M1/M2 ratio in epididymal fat were unaltered. Under HFHS chow, Gal-9^−/− mice receiving Gal-9^−/− or Gal-9^wt/wt bone marrow-derived cells (BMCs) demonstrated significantly lower body weight compared with Gal-9^wt/wt mice receiving Gal-9^−/− BMCs. We identified the binding between Gal-9 and peroxiredoxin-2 (PRDX2) in sugar chain-independent manner by nanoLC-MS/MS, immunoprecipitation, and pull-down assay. In 3T3L1 adipocytes, Gal-9 knockdown shifts PRDX2 monomer (reduced form) dominant from PRDX2 dimer (oxidized form) under oxidative stress with H₂O₂. The inhibition of Gal-9 in adipocytes may be a new therapeutic approach targeting the oxidative stress and subsequent glucose intolerance in obesity.

DOI： 10.1038/s41598-021-85080-1

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Other Link： http://www.nature.com/articles/s41598-021-85080-1
Upregulation of Mir342 in Diet-Induced Obesity Mouse and the Hypothalamic Appetite Control Reviewed

Dongxiao Zhang, Satoshi Yamaguchi, Xinhao Zhang, Boxuan Yang, Naoko Kurooka, Ryosuke Sugawara, Haya Hamed H. Albuayjan, Atsuko Nakatsuka, Jun Eguchi, Takeshi Y. Hiyama, Atsunori Kamiya, Jun Wada

Frontiers in Endocrinology 12 2021.8

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Publishing type：Research paper (scientific journal) Publisher：Frontiers Media SA

DOI： 10.3389/fendo.2021.727915

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Current Status of Familial LCAT Deficiency in Japan Reviewed

Masayuki Kuroda, Hideaki Bujo, Koutaro Yokote, Takeyoshi Murano, Takashi Yamaguchi, Masatsune Ogura, Katsunori Ikewaki, Masahiro Koseki, Yasuo Takeuchi, Atsuko Nakatsuka, Mika Hori, Kota Matsuki, Takashi Miida, Shinji Yokoyama, Jun Wada, Mariko Harada-Shiba

Journal of Atherosclerosis and Thrombosis 28 ( 7 ) 679 - 691 2021.7

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Language：English Publishing type：Research paper (scientific journal) Publisher：Japan Atherosclerosis Society

Lecithin cholesterol acyltransferase (LCAT) is a lipid-modification enzyme that catalyzes the transfer of the acyl chain from the second position of lecithin to the hydroxyl group of cholesterol (FC) on plasma lipoproteins to form cholesteryl acylester and lysolecithin. Familial LCAT deficiency is an intractable autosomal recessive disorder caused by inherited dysfunction of the LCAT enzyme. The disease appears in two different phenotypes depending on the position of the gene mutation: familial LCAT deficiency (FLD, OMIM 245900) that lacks esterification activity on both HDL and ApoB-containing lipoproteins, and fish-eye disease (FED, OMIM 136120) that lacks activity only on HDL. Impaired metabolism of cholesterol and phospholipids due to LCAT dysfunction results in abnormal concentrations, composition and morphology of plasma lipoproteins and further causes ectopic lipid accumulation and/or abnormal lipid composition in certain tissues/cells, and serious dysfunction and complications in certain organs. Marked reduction of plasma HDL-cholesterol (HDL-C) and corneal opacity are common clinical manifestations of FLD and FED. FLD is also accompanied by anemia, proteinuria and progressive renal failure that eventually requires hemodialysis. Replacement therapy with the LCAT enzyme should prevent progression of serious complications, particularly renal dysfunction and corneal opacity. A clinical research project aiming at gene/cell therapy is currently underway.

DOI： 10.5551/jat.rv17051

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Novel Urinary Glycan Biomarkers Predict Cardiovascular Events in Patients With Type 2 Diabetes: A Multicenter Prospective Study With 5-Year Follow Up (U-CARE Study 2) Reviewed International journal

Koki Mise, Mariko Imamura, Satoshi Yamaguchi, Mayu Watanabe, Chigusa Higuchi, Akihiro Katayama, Satoshi Miyamoto, Haruhito A. Uchida, Atsuko Nakatsuka, Jun Eguchi, Kazuyuki Hida, Tatsuaki Nakato, Atsuhito Tone, Sanae Teshigawara, Takashi Matsuoka, Shinji Kamei, Kazutoshi Murakami, Ikki Shimizu, Katsuhiro Miyashita, Shinichiro Ando, Tomokazu Nunoue, Michihiro Yoshida, Masao Yamada, Kenichi Shikata, Jun Wada

Frontiers in Cardiovascular Medicine 8 668059 - 668059 2021.5

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Language：English Publishing type：Research paper (scientific journal) Publisher：Frontiers Media SA

<bold>Background:</bold> Although various biomarkers predict cardiovascular event (CVE) in patients with diabetes, the relationship of urinary glycan profile with CVE in patients with diabetes remains unclear.

<bold>Methods:</bold> Among 680 patients with type 2 diabetes, we examined the baseline urinary glycan signals binding to 45 lectins with different specificities. Primary outcome was defined as CVE including cardiovascular disease, stroke, and peripheral arterial disease.

<bold>Results:</bold> During approximately a 5-year follow-up period, 62 patients reached the endpoint. Cox proportional hazards analysis revealed that urinary glycan signals binding to two lectins were significantly associated with the outcome after adjustment for known indicators of CVE and for false discovery rate, as well as increased model fitness. Hazard ratios for these lectins (+1 SD for the glycan index) were UDA (recognizing glycan: mixture of Man5 to Man9): 1.78 (95% CI: 1.24–2.55, <italic>P</italic> = 0.002) and Calsepa [High-Man (Man2–6)]: 1.56 (1.19–2.04, <italic>P</italic> = 0.001). Common glycan binding to these lectins was high-mannose type of <italic>N</italic>-glycans. Moreover, adding glycan index for UDA to a model including known confounders improved the outcome prediction [Difference of Harrel's C-index: 0.028 (95% CI: 0.001–0.055, <italic>P</italic> = 0.044), net reclassification improvement at 5-year risk increased by 0.368 (0.045–0.692, <italic>P</italic> = 0.026), and the Akaike information criterion and Bayesian information criterion decreased from 725.7 to 716.5, and 761.8 to 757.2, respectively].

<bold>Conclusion:</bold> The urinary excretion of high-mannose glycan may be a valuable biomarker for improving prediction of CVE in patients with type 2 diabetes, and provides the rationale to explore the mechanism underlying abnormal <italic>N</italic>-glycosylation occurring in patients with diabetes at higher risk of CVE.

<bold>Trial Registration:</bold> This study was registered with the University Hospital Medical Information Network on June 26, 2012 (Clinical trial number: UMIN000011525, URL: <ext-link>https://upload.umin.ac.jp/cgi-open-bin/ctr_e/ctr_view.cgi?recptno=R000013482</ext-link>).

DOI： 10.3389/fcvm.2021.668059

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Adipocyte-Specific Inhibition of Mir221/222 Ameliorates Diet-Induced Obesity Through Targeting Ddit4. Reviewed International journal

Satoshi Yamaguchi, Dongxiao Zhang, Akihiro Katayama, Naoko Kurooka, Ryosuke Sugawara, Haya Hamed Hassan Albuayjan, Atsuko Nakatsuka, Jun Eguchi, Jun Wada

Frontiers in endocrinology 12 750261 - 750261 2021

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MicroRNAs expressed in adipocytes are involved in transcriptional regulation of target mRNAs in obesity, but miRNAs critically involved in this process is not well characterized. Here, we identified upregulation of miR-221-3p and miR-222-3p in the white adipose tissues in C57BL/6 mice fed with high fat-high sucrose (HFHS) chow by RNA sequencing. Mir221 and Mir222 are paralogous genes and share the common seed sequence and Mir221/222AdipoKO mice fed with HFHS chow demonstrated resistance to the development of obesity compared with Mir221/222flox/y . Ddit4 is a direct target of Mir221 and Mir222, and the upregulation of Ddit4 in Mir221/222AdipoKO was associated with the suppression of TSC2 (tuberous sclerosis complex 2)/mammalian target of rapamycin complex 1 (mTORC1)/S6K (ribosomal protein S6 kinase) pathway. The overexpression of miR-222-3p linked to enhanced adipogenesis, and it may be a potential candidate for miRNA-based therapy.

DOI： 10.3389/fendo.2021.750261

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Current diagnosis and management of primary chylomicronemia

Hiroaki Okazaki, Takanari Gotoda, Masatsune Ogura, Shun Ishibashi, Kyoko Inagaki, Hiroyuki Daida, Toshio Hayashi, Mika Hori, Daisaku Masuda, Kota Matsuki, Shinji Yokoyama, Mariko Harada-Shiba, Hitoshi Shimano, Koutaro Yokote, Hideaki Bujo, Shizuya Yamashita, Kazuhisa Tsukamoto, Katsunori Ikewaki, Kazushige Dobashi, Yoshihiro Miyamoto, Misa Takegami, Yoshiki Sekijima, Yasushi Ishigaki, Atsushi Nohara, Shingo Koyama, Koh Ono, Masahiro Koseki, Manabu Takahashi, Kimitoshi Nakamura, Takashi Miida, Masa Aki Kawashiri, Tetsuo Minamino, Sachiko Okazaki, Hayato Tada, Jun Wada, Hirotoshi Ohmura, Masashi Yamamoto, Yasuo Takeuchi, Atsuko Nakatsuka, Satoshi Hirayama, Masayuki Kuroda, Takashi Yamaguchi, Takeyoshi Murano

Journal of Atherosclerosis and Thrombosis 28 ( 9 ) 883 - 904 2021

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DOI： 10.5551/jat.RV17054

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Dysfunction of CD8 + PD-1 + T cells in type 2 diabetes caused by the impairment of metabolism-immune axis International journal

Ichiro Nojima, Shingo Eikawa, Nahoko Tomonobu, Yoshiko Hada, Nobuo Kajitani, Sanae Teshigawara, Satoshi Miyamoto, Atsuhito Tone, Haruhito A. Uchida, Atsuko Nakatsuka, Jun Eguchi, Kenichi Shikata, Heiichiro Udono, Jun Wada

Scientific Reports 10 ( 1 ) 14928 - 14928 2020.12

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Language：English Publishing type：Research paper (scientific journal) Publisher：Springer Science and Business Media LLC

<title>Abstract</title>
The metabolic changes and dysfunction in CD8 + T cells may be involved in tumor progression and susceptibility to virus infection in type 2 diabetes (T2D). In C57BL/6JJcl mice fed with high fat-high sucrose chow (HFS), multifunctionality of CD8 + splenic and tumor-infiltrating lymphocytes (TILs) was impaired and associated with enhanced tumor growth, which were inhibited by metformin. In CD8 + splenic T cells from the HFS mice, glycolysis/basal respiration ratio was significantly reduced and reversed by metformin. In the patients with T2D (DM), multifunctionality of circulating CD8 + PD-1 + T cells stimulated with PMA/ionomycin as well as with HLA-A*24:02 CMV peptide was dampened, while metformin recovered multifunctionality. Both glycolysis and basal respiration were reduced in DM, and glycolysis was increased by metformin. The disturbance of the link between metabolism and immune function in CD8 + PD-1 + T cells in T2D was proved by recovery of antigen-specific and non-specific cytokine production via metformin-mediated increase in glycolytic activity.

DOI： 10.1038/s41598-020-71946-3

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Other Link： http://www.nature.com/articles/s41598-020-71946-3
High expression of a vascular stricture‐related marker is predictive of an early response to tolvaptan, and a low fractional excretion of sodium is predictive of a poor long‐term survival after tolvaptan administration for liver cirrhosis International journal

Takuya Adachi, Akinobu Takaki, Shuichi Sato, Hiroshi Tobita, Haruhiko Kobashi, Masaru Kinomura, Atsuko Nakatsuka, Atsushi Oyama, Nozomu Wada, Masahiro Sakata, Yasuto Takeuchi, Tetsuya Yasunaka, Hideki Onishi, Hidenori Shiraha, Hiroyuki Okada

Hepatology Research 50 ( 12 ) 1347 - 1354 2020.12

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Language：English Publishing type：Research paper (scientific journal) Publisher：Wiley

AIM: Tolvaptan is a newly available diuretic that has a specific function in water reabsorption inhibition. Given that spironolactone or furosemide induces the aggravation of cirrhotic hyponatremia and dehydration, tolvaptan affects the management strategy of liver cirrhosis. Representative predictive markers of its response include renal function-related markers such as urea nitrogen or creatinine. However, vascular function-related markers have not been well investigated. We investigated the effect of the vascular function-related marker asymmetric dimethylarginine (ADMA) and the effective arterial blood volume (EABV) marker, fractional excretion of sodium (FENa), on the early tolvaptan response and survival in liver cirrhosis. METHODS: We prospectively recruited 49 patients who required add-on tolvaptan for refractory ascites or edema. Laboratory data were obtained immediately before and 1 day after tolvaptan administration. Patients exhibiting >1.5 kg weight loss after 1 week were categorized as early responders to tolvaptan. Patients were followed for a median of 200 days and were assessed for survival. RESULTS: Early responders showed lower creatinine levels (<1.0 mg/dL), and higher ADMA levels (≥0.61 nmol/mL) than others in a multivariate analysis. Patients with a shorter survival were positive for hepatocellular carcinoma and had a low FENa (<0.35%). CONCLUSION: Early responders showed higher ADMA levels reflecting vascular stricture, suggesting that higher vascular tonus is required for a tolvaptan early response. Patients with a shorter survival showed a lower FENa, reflecting a lower EABV and suggesting that adequate EABV is required for the prolonged survival after tolvaptan administration.

DOI： 10.1111/hepr.13573

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Other Link： https://onlinelibrary.wiley.com/doi/full-xml/10.1111/hepr.13573
当院における糖尿病性腎症の進展抑制を目指した取り組み

長田麻里, 片山晶博, 大橋睦子, 高橋絢子, 庄野三友紀, 江口潤, 中司敦子, 宮本聡, 長谷川祐子, 和田淳

糖尿病 63 ( 9 ) 650 - 650 2020.9

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当院におけるTime-In-Range(TIR)とHbA1cとの関連についての検討

片山晶博, 野島一郎, 樋口千草, 渡邉真由, 宮本聡, 中司敦子, 江口潤, 四方賢一, 和田淳

糖尿病 63 ( Suppl.1 ) S - 220 2020.8

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尿細管間質障害におけるHSPA1Lの意義

中司敦子, 江口潤, 和田淳

日本腎臓学会誌 62 ( 4 ) 284 - 284 2020.7

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The hypoglycemia-prevention effect of sensor-augmented pump therapy with predictive low glucose management in Japanese patients with type 1 diabetes mellitus: a short-term study

Akihiro Katayama, Atsuhito Tone, Mayu Watanabe, Sanae Teshigawara, Satoshi Miyamoto, Jun Eguchi, Atsuko Nakatsuka, Kenichi Shikata, Jun Wada

Diabetology International 11 ( 2 ) 97 - 104 2020.4

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Aims/introduction: The predictive low glucose management (PLGM) system was introduced in March 2018 in Japan. Although there are some reports demonstrating the benefit of PLGM in preventing hypoglycemia, no data are currently available in Japanese patients with type 1 diabetes mellitus (T1DM). The aim of the present study is to evaluate the effect of PLGM with sensor-augmented pump therapy in the prevention of hypoglycemia in Japanese patients. Materials and methods: We included 16 patients with T1DM who used the MiniMed®640G system after switching from the MiniMed®620G system. We retrospectively analysed the data of the continuous glucose monitoring system in 1 month after switching to MiniMed®640G. Results: The area under the curve (AUC) of hypoglycemia of < 70 mg/dL was lowered from 0.42 ± 0.43 mg/dL day to 0.18 ± 0.18 mg/dL day (P = 0.012). Correspondingly, the duration of severe hypoglycemia (< 54 mg/dL) was reduced significantly from 15.3 ± 21.7 min/day to 4.8 ± 6.9 min/day (P = 0.019). The duration of hypoglycemia was reduced, but the reduction was not significant. Regarding the AUC for hyperglycemia > 180 mg/dL and the duration of hyperglycemia did not change. With the PLGM function, 79.3% of the predicted hypoglycemic events were avoided. Conclusions: The hypoglycemia avoidance rate was comparable to those in previous reports. In addition, we demonstrated that PLGM can markedly suppress severe hypoglycemia without deteriorating glycemic control in Japanese T1DM patients. It is necessary to further investigate the effective use of the PLGM feature such as establishing a lower limit and the timing of resumption.

DOI： 10.1007/s13340-019-00408-7

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脂質異常症難病のすべてがわかる! 低HDL-C血症の診断の進め方 LCAT欠損症とタンジール病

武城英明, 小関正博, 黒田正幸, 村野武義, 中司敦子, 和田淳, 竹内康雄, 石川耕, 横手幸太郎, 山下静也

日本動脈硬化学会総会プログラム・抄録集 51回 S12 - 4 2019.7

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Fetuin-Aの糖尿病腎症進展における役割

三瀬広記, 中司敦子, 山口哲志, 勅使川原早苗, 田邊克幸, 江口潤, 和田淳

糖尿病 62 ( Suppl.1 ) S - 202 2019.4

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2型糖尿病患者における尿中糖鎖排泄量と腎・心血管イベントおよび総死亡との関連の検討 Reviewed

今村麻理子, 三瀬広記, 中塔辰明, 清水一紀, 安藤晋一郎, 松岡孝, 宮下雄博, 肥田和之, 江口潤, 中司敦子, 四方賢一, 和田淳

糖尿病 62 ( 2 ) 113 - 113 2019.2

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GPIHBP1 autoantibody syndrome during interferon β1a treatment. Reviewed

Eguchi J, Miyashita K, Fukamachi I, Nakajima K, Murakami M, Kawahara Y, Yamashita T, Ohta Y, Abe K, Nakatsuka A, Mino M, Takase S, Okazaki H, Hegele RA, Ploug M, Hu X, Wada J, Young SG, Beigneux AP

Journal of clinical lipidology 13 ( 1 ) 62 - 69 2019.1

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DOI： 10.1016/j.jacl.2018.10.004

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A retrospective observational study on the effects of switching from conventional insulin pump to sensor-augmented pump (SAP) therapy

Satoshi Yamaguchi, Atsuhito Tone, Sanae Teshigawara, Mayu Watanabe, Akihiro Katayama, Satoshi Miyamoto, Jun Eguchi, Atsuko Nakatsuka, Chigusa Higuchi, Daisuke Ogawa, Kenichi Shikata, Jun Wada

Journal of the Japan Diabetes Society 62 ( 5 ) 315 - 321 2019

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DOI： 10.11213/tonyobyo.62.315

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Acquired partial lipoatrophy as graft-versus-host disease and treatment with metreleptin: two case reports. Reviewed International journal

Shibata Y, Nakatsuka A, Eguchi J, Miyamoto S, Masuda Y, Awazawa M, Takaki A, Yoshida R, Yagi T, Wada J

Journal of medical case reports 12 ( 1 ) 368 - 368 2018.12

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INTRODUCTION: Acquired partial lipoatrophy has been reported after bone marrow transplantation during childhood; however, no adult cases have previously been reported. We herein report two adult cases of acquired partial lipoatrophy after transplantation. CASE PRESENTATION: A 28-year-old Japanese woman developed diabetic ketoacidosis and received insulin therapy after bone marrow transplantation. She manifested partial lipoatrophy of the extremities, prominent insulin resistance, hyperglycemia, hypertriglyceridemia, and fatty liver. A 40-year-old Japanese woman underwent liver transplantation from a living donor for alcoholic liver disease after abstinence from alcohol. She newly developed non-alcoholic steatohepatitis and diabetes. Non-alcoholic steatohepatitis progressed to liver failure, and a second liver transplantation from a brain-dead donor was performed at 42 years of age. She demonstrated loss of subdermal fat of the upper and lower extremities, prominent insulin resistance, hyperglycemia, and hypertriglyceridemia. In both cases, the injection of recombinant methionyl human leptin reversed all of the metabolic abnormalities. CONCLUSIONS: Acquired partial lipoatrophy after transplantation is a manifestation of chronic graft-versus-host disease in adults. This entity is associated with diabetes with prominent insulin resistance and severe hypertriglycemia and can be successfully treated with metreleptin for the long term.

DOI： 10.1186/s13256-018-1901-y

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Identification of Novel Urinary Biomarkers for Predicting Renal Prognosis in Patients With Type 2 Diabetes by Glycan Profiling in a Multicenter Prospective Cohort Study: U-CARE Study 1. Reviewed International journal

Mise K, Imamura M, Yamaguchi S, Teshigawara S, Tone A, Uchida HA, Eguchi J, Nakatsuka A, Ogawa D, Yoshida M, Yamada M, Shikata K, Wada J

Diabetes care 41 ( 8 ) 1765 - 1775 2018.8

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OBJECTIVE: Because quantifying glycans with complex structures is technically challenging, little is known about the association of glycosylation profiles with the renal prognosis in diabetic kidney disease (DKD). RESEARCH DESIGN AND METHODS: In 675 patients with type 2 diabetes, we assessed the baseline urinary glycan signals binding to 45 lectins with different specificities. The end point was a decrease of estimated glomerular filtration rate (eGFR) by ≥30% from baseline or dialysis for end-stage renal disease. RESULTS: During a median follow-up of 4.0 years, 63 patients reached the end point. Cox proportional hazards analysis revealed that urinary levels of glycans binding to six lectins were significantly associated with the outcome after adjustment for known indicators of DKD, although these urinary glycans, except that for DBA, were highly correlated with baseline albuminuria and eGFR. Hazard ratios for these lectins were (+1 SD for the glycan index) as follows: SNA (recognizing glycan Siaα2-6Gal/GalNAc), 1.42 (95% CI 1.14-1.76); RCA120 (Galβ4GlcNAc), 1.28 (1.01-1.64); DBA (GalNAcα3GalNAc), 0.80 (0.64-0.997); ABA (Galβ3GalNAc), 1.29 (1.02-1.64); Jacalin (Galβ3GalNAc), 1.30 (1.02-1.67); and ACA (Galβ3GalNAc), 1.32 (1.04-1.67). Adding these glycan indexes to a model containing known indicators of progression improved prediction of the outcome (net reclassification improvement increased by 0.51 [0.22-0.80], relative integrated discrimination improvement increased by 0.18 [0.01-0.35], and the Akaike information criterion decreased from 296 to 287). CONCLUSIONS: The urinary glycan profile identified in this study may be useful for predicting renal prognosis in patients with type 2 diabetes. Additional investigation of glycosylation changes and urinary glycan excretion in DKD is needed.

DOI： 10.2337/dc18-0030

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岡山大学病院における肥満外科治療の導入

香川俊輔, 黒田新士, 菊地覚次, 桑田和也, 西崎正彦, 利根淳仁, 中司敦子, 江口潤, 和田淳, 小林求, 藤原俊義

日本肥満症治療学会学術集会プログラム・抄録集 36回 129 - 129 2018.6

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1型糖尿病合併妊婦における妊娠期間中の体重変化とインスリン所要量の検討

勅使川原早苗, 利根淳仁, 山口哲志, 渡邉真由, 三瀬広記, 野島一郎, 高橋寛子, 柴田祐介, 中司敦子, 江口潤, 和田淳

糖尿病 61 ( Suppl.1 ) S - 311 2018.4

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肥満・糖尿病による近位尿細管細胞障害とvaspinの細胞保護作用機序の解明

中司敦子, 山口哲志, 柴田祐助, 高橋寛子, 三瀬広記, 勅使川原早苗, 江口潤, 和田淳

糖尿病 60 ( Suppl.1 ) S - 259 2017.4

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Serum-inducible protein (IP)-10 is a disease progression-related marker for non-alcoholic fatty liver disease Reviewed

Nozomu Wada, Akinobu Takaki, Fusao Ikeda, Tetsuya Yasunaka, Masahiro Onji, Kazuhiro Nouso, Atsuko Nakatsuka, Jun Wada, Kazuko Koike, Koji Miyahara, Hidenori Shiraha, Kazuhide Yamamoto, Hiroyuki Okada

HEPATOLOGY INTERNATIONAL 11 ( 1 ) 115 - 124 2017.1

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DOI： 10.1007/s12072-016-9773-y

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Microinflammation and organelle dysfunctions in diabetic nephropathy. Reviewed

Nakatsuka A, Wada J

Nihon Jinzo Gakkai shi 59 ( 2 ) 58 - 64 2017

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Mitochondrial Dynamics and Mitochondrial Dysfunction in Diabetes Reviewed

Jun Wada, Atsuko Nakatsuka

ACTA MEDICA OKAYAMA 70 ( 3 ) 151 - 158 2016.6

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DOI： 10.18926/AMO/54413

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Antiobesity Action of ACAM by Modulating the Dynamics of Cell Adhesion and Actin Polymerization in Adipocytes Reviewed

Kazutoshi Murakami, Jun Eguchi, Kazuyuki Hida, Atsuko Nakatsuka, Akihiro Katayama, Miwa Sakurai, Haruki Choshi, Masumi Furutani, Daisuke Ogawa, Kohji Takei, Fumio Otsuka, Jun Wada

DIABETES 65 ( 5 ) 1255 - 1267 2016.5

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DOI： 10.2337/db15-1304

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糖尿病性腎症におけるVaspinの意義

中司敦子, 三瀬広記, 江口潤, 和田淳

日本腎臓学会誌 58 ( 3 ) 262 - 262 2016.5

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Insufficiency of phosphatidylethanolamine N-methyltransferase is risk for lean non-alcoholic steatohepatitis Reviewed

Atsuko Nakatsuka, Makoto Matsuyama, Satoshi Yamaguchi, Akihiro Katayama, Jun Eguchi, Kazutoshi Murakami, Sanae Teshigawara, Daisuke Ogawa, Nozomu Wada, Tetsuya Yasunaka, Fusao Ikeda, Akinobu Takaki, Eijiro Watanabe, Jun Wada

SCIENTIFIC REPORTS 6 21721 2016.2

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DOI： 10.1038/srep21721

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Beneficial impact of Gpnmb and its significance as a biomarker in nonalcoholic steatohepatitis Reviewed

Akihiro Katayama, Atsuko Nakatsuka, Jun Eguchi, Kazutoshi Murakami, Sanae Teshigawara, Motoko Kanzaki, Tomokazu Nunoue, Kazuyuki Hida, Nozomu Wada, Tetsuya Yasunaka, Fusao Ikeda, Akinobu Takaki, Kazuhide Yamamoto, Hiroshi Kiyonari, Hirofumi Makino, Jun Wada

SCIENTIFIC REPORTS 5 16920 2015.11

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DOI： 10.1038/srep16920

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Translocase of inner mitochondrial membrane 44 alters the mitochondrial fusion and fission dynamics and protects from type 2 diabetes Reviewed

Yu Wang, Akihiro Katayama, Takahiro Terami, Xiaoying Han, Tomokazu Nunoue, Dongxiao Zhang, Sanae Teshigawara, Jun Eguchi, Atsuko Nakatsuka, Kazutoshi Murakami, Daisuke Ogawa, Yasuhide Furuta, Hirofumi Makino, Jun Wada

METABOLISM-CLINICAL AND EXPERIMENTAL 64 ( 6 ) 677 - 688 2015.6

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DOI： 10.1016/j.metabol.2015.02.004

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Identification of Circulating miR-101, miR-375 and miR-802 as Biomarkers for Type 2 Diabetes Reviewed

Chigusa Higuchi, Atsuko Nakatsuka, Jun Eguchi, Sanae Teshigawara, Motoko Kanzaki, Akihiro Katayama, Satoshi Yamaguchi, Naoto Takahashi, Kazutoshi Murakami, Daisuke Ogawa, Sakiko Sasaki, Hirofumi Makino, Jun Wada

METABOLISM-CLINICAL AND EXPERIMENTAL 64 ( 4 ) 489 - 497 2015.4

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DOI： 10.1016/j.metabol.2014.12.003

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Long-Term Treatment with the Sodium Glucose Cotransporter 2 Inhibitor, Dapagliflozin, Ameliorates Glucose Homeostasis and Diabetic Nephropathy in db/db Mice Reviewed

Naoto Terami, Daisuke Ogawa, Hiromi Tachibana, Takashi Hatanaka, Jun Wada, Atsuko Nakatsuka, Jun Eguchi, Chikage Sato Horiguchi, Naoko Nishii, Hiroshi Yamada, Kohji Takei, Hirofumi Makino

PLOS ONE 9 ( 6 ) e100777 2014.6

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DOI： 10.1371/journal.pone.0100777

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Serum vaspin levels are associated with physical activity or physical fitness in Japanese: a pilot study Reviewed

Nobuyuki Miyatake, Jun Wada, Atsuko Nakatsuka, Noriko Sakano, Sanae Teshigawara, Motohiko Miyachi, Izumi Tabata, Takeyuki Numata

ENVIRONMENTAL HEALTH AND PREVENTIVE MEDICINE 19 ( 3 ) 200 - 206 2014.5

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DOI： 10.1007/s12199-013-0375-1

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Pemt Deficiency Ameliorates Endoplasmic Reticulum Stress in Diabetic Nephropathy Reviewed

Mayu Watanabe, Atsuko Nakatsuka, Kazutoshi Murakami, Kentaro Inoue, Takahiro Terami, Chigusa Higuchi, Akihiro Katayama, Sanae Teshigawara, Jun Eguchi, Daisuke Ogawa, Eijiro Watanabe, Jun Wada, Hirofumi Makino

PLOS ONE 9 ( 3 ) e92647 2014.3

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DOI： 10.1371/journal.pone.0092647

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Metallothionein deficiency exacerbates diabetic nephropathy in streptozotocin-induced diabetic mice Reviewed

Hiromi Tachibana, Daisuke Ogawa, Norio Sogawa, Masato Asanuma, Ikuko Miyazaki, Naoto Terami, Takashi Hatanaka, Chikage Sato Horiguchi, Atsuko Nakatsuka, Jun Eguchi, Jun Wada, Hiroshi Yamada, Kohji Takei, Hirofumi Makino

American Journal of Physiology - Renal Physiology 306 ( 1 ) F105 - F115 2014.1

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DOI： 10.1152/ajprenal.00034.2013

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Metallothionein deficiency exacerbates diabetic nephropathy in streptozotocin-induced diabetic mice Reviewed

Hiromi Tachibana, Daisuke Ogawa, Norio Sogawa, Masato Asanuma, Ikuko Miyazaki, Naoto Terami, Takashi Hatanaka, Chikage Sato Horiguchi, Atsuko Nakatsuka, Jun Eguchi, Jun Wada, Hiroshi Yamada, Kohji Takei, Hirofumi Makino

AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY 306 ( 1 ) F105 - F115 2014.1

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DOI： 10.1152/ajprenal.00034.2013

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Nuclear Hormone Receptor Expression in Mouse Kidney and Renal Cell Lines Reviewed

Daisuke Ogawa, Jun Eguchi, Jun Wada, Naoto Terami, Takashi Hatanaka, Hiromi Tachibana, Atsuko Nakatsuka, Chikage Sato Horiguchi, Naoko Nishii, Hirofumi Makino

PLOS ONE 9 ( 1 ) e85594 2014.1

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DOI： 10.1371/journal.pone.0085594

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Comparison of New Preservation Solutions, HN-1 and University of Wisconsin Solution, in Pancreas Preservation for Porcine Islet Isolation. Reviewed International journal

Katayama A, Noguchi H, Kuise T, Nakatsuka A, Hirota D, Kataoka HU, Kawai T, Inoue K, Imagawa N, Saitoh I, Noguchi Y, Watanabe M, Wada J, Fujiwara T

Cell medicine 6 ( 1-2 ) 3 - 8 2013.12

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For pancreatic islet transplantation, maintaining organ viability after pancreas procurement is critical and a major determinant for better graft function and survival. University of Wisconsin (UW) solution is currently the gold standard for abdominal organ preservation and the pancreas in particular. However, in the use of UW preservation solution for islet transplantation, there are disadvantages to be overcome, such as the inhibition of collagenase activity during pancreatic digestion. In this study, we compared UW solution with HN-1 solution in pancreas preservation for islet isolation. Islet yield was significantly greater in the HN-1 group than the UW group both before and after purification. In the in vitro assay, the adenosine triphosphate content in cultured islets was significantly higher in the HN-1 group than in the UW group. Furthermore, in streptozotocin-induced diabetic nude mice, the islet graft function of the HN-1 group was superior to that of the UW group. We concluded that the use of HN-1 solution is a promising approach for optimal pancreas preservation in islet transplantation.

DOI： 10.3727/215517913X674171

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Comparison of Incubation Solutions Prior to the Purification of Porcine Islet Cells. Reviewed International journal

Kawai T, Noguchi H, Kuise T, Nakatsuka A, Katayama A, Imagawa N, Kataoka HU, Saitoh I, Noguchi Y, Watanabe M, Fujiwara T

Cell medicine 6 ( 1-2 ) 9 - 14 2013.12

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For pancreatic islet transplantation, one of the most important steps of islet isolation is islet purification. The most common method of islet purification is density gradient centrifugation because there are differences in density between islets and acinar tissue. However, the density of islets/acinar tissue depends on several conditions, such as the incubation time before purification and the osmolality of the preincubation solution. In this study, we evaluated the impact of using two different preincubation solutions before purification. We used the University of Wisconsin (UW) solution and a new preservation solution (HN-1), which we recently developed. There were no significant differences between the two solutions in terms of the islet yield, rate of viability, and purity or stimulation index after purification. There were also no differences in the attainability and suitability of posttransplantation normoglycemia. Our study shows that the HN-1 solution is equivalent to the UW solution for preincubation before islet purification.

DOI： 10.3727/215517913X674180

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Urinary angiotensinogen is a marker for tubular injuries in patients with type 2 diabetes Reviewed

Takahiro Terami, Jun Wada, Kentaro Inoue, Atsuko Nakatsuka, Daisuke Ogawa, Sanae Teshigawara, Kazutoshi Murakami, Akihiro Katayama, Jun Eguchi, Hirofumi Makino

International Journal of Nephrology and Renovascular Disease 6 233 - 240 2013.10

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DOI： 10.2147/IJNRD.S51829

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Urinary Fetuin-A Is a Novel Marker for Diabetic Nephropathy in Type 2 Diabetes Identified by Lectin Microarray Reviewed

Kentaro Inoue, Jun Wada, Jun Eguchi, Atsuko Nakatsuka, Sanae Teshigawara, Kazutoshi Murakami, Daisuke Ogawa, Takahiro Terami, Akihiro Katayama, Atsuhito Tone, Izumi Iseda, Kazuyuki Hida, Masao Yamada, Tomohisa Ogawa, Hirofumi Makino

PLoS ONE 8 ( 10 ) e77118 2013.10

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DOI： 10.1371/journal.pone.0077118

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Nuclear Hormone Receptor Expression in Mouse Kidney and Renal Cell Lines

Naoto Terami, Daisuke Ogawa, Jun Eguchi, Hiromi Tachibana, Chikage Sato-Horiguchi, Takashi Hatanaka, Atsuko Nakatsuka, Jun Wada, Hirofumi Makino

DIABETES 62 A134 - A134 2013.7

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Phosphatidylethanolamine N-Methyltransferase (PEMT) Deficiency Protects from Obesity and Insulin Resistance but Promote Steatoheptitis With Tumorigenesis Reviewed

Atsuko Nakatsuka, Jun Wada, Kazutoshi Murakami, Takahiro Terami, Jun Eguchi, Daisuke Ogawa, Hirofumi Makino

DIABETES 62 A529 - A529 2013.7

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Cell Cycle Abnormality in Metabolic Syndrome and Nuclear Receptors as an Emerging Therapeutic Target Reviewed

Atsuko Nakatsuka, Jun Wada, Hirofumi Makino

ACTA MEDICA OKAYAMA 67 ( 3 ) 129 - 134 2013.6

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DOI： 10.18926/AMO/50405

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Visceral adipose tissue-derived serine proteinase inhibitor inhibits apoptosis of endothelial cells as a ligand for the cell-surface GRP78/voltage-dependent anion channel complex (vol 112, pg 771, 2013) Reviewed

A. Nakatsuka, J. Wada, I. Iseda

CIRCULATION RESEARCH 112 ( 9 ) E98 - E98 2013.4

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DOI： 10.1161/RES.0b013e31829329f8

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【内分泌ホルモンのすべて】(第15章)脂肪由来のホルモンバスピン

和田淳, 勅使川原早苗, 中司敦子

内分泌・糖尿病・代謝内科 36 ( Suppl.4 ) 466 - 471 2013.4

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Visceral Adipose Tissue-derived Serine Proteinase Inhibitor Inhibits Apoptosis of Endothelial Cells as a Ligand for the Cell-Surface GRP78/Voltage-dependent Anion Channel Complex Reviewed

Atsuko Nakatsuka, Jun Wada, Izumi Iseda, Sanae Teshigawara, Kanji Higashio, Kazutoshi Murakami, Motoko Kanzaki, Kentaro Inoue, Takahiro Terami, Akihiro Katayama, Kazuyuki Hida, Jun Eguchi, Daisuke Ogawa, Yasushi Matsuki, Ryuji Hiramatsu, Hideo Yagita, Shigeru Kakuta, Yoichiro Iwakura, Hirofumi Makino

CIRCULATION RESEARCH 112 ( 5 ) 771 - + 2013.3

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DOI： 10.1161/CIRCRESAHA.111.300049

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Serum galectin-9 levels are elevated in the patients with type 2 diabetes and chronic kidney disease Reviewed

Yuko Kurose, Jun Wada, Motoko Kanzaki, Sanae Teshigawara, Atsuko Nakatsuka, Kazutoshi Murakami, Kentaro Inoue, Takahiro Terami, Akihiro Katayama, Mayu Watanabe, Chigusa Higuchi, Jun Eguchi, Nobuyuki Miyatake, Hirofumi Makino

BMC NEPHROLOGY 14 23 2013.1

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DOI： 10.1186/1471-2369-14-23

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The serum vaspin levels are reduced in Japanese chronic hemodialysis patients Reviewed

Junko Inoue, Jun Wada, Sanae Teshigawara, Kazuyuki Hida, Atsuko Nakatsuka, Yuji Takatori, Shoichirou Kojo, Shigeru Akagi, Kazushi Nakao, Nobuyuki Miyatake, John F. McDonald, Hirofumi Makino

BMC NEPHROLOGY 13 163 2012.12

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DOI： 10.1186/1471-2369-13-163

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Vaspin Is an Adipokine Ameliorating ER Stress in Obesity as a Ligand for Cell-Surface GRP78/MTJ-1 Complex Reviewed

Atsuko Nakatsuka, Jun Wada, Izumi Iseda, Sanae Teshigawara, Kanji Higashio, Kazutoshi Murakami, Motoko Kanzaki, Kentaro Inoue, Takahiro Terami, Akihiro Katayama, Kazuyuki Hida, Jun Eguchi, Chikage Sato Horiguchi, Daisuke Ogawa, Yasushi Matsuki, Ryuji Hiramatsu, Hideo Yagita, Shigeru Kakuta, Yoichiro Iwakura, Hirofumi Makino

DIABETES 61 ( 11 ) 2823 - 2832 2012.11

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DOI： 10.2337/db12-0232

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Hydrogen-rich water prevents progression of nonalcoholic steatohepatitis and accompanying hepatocarcinogenesis in mice Reviewed

Daisuke Kawai, Akinobu Takaki, Atsuko Nakatsuka, Jun Wada, Naofumi Tamaki, Tetsuya Yasunaka, Kazuko Koike, Ryuichiro Tsuzaki, Kazuyuki Matsumoto, Yasuhiro Miyake, Hidenori Shiraha, Manabu Morita, Hirofumi Makino, Kazuhide Yamamoto

HEPATOLOGY 56 ( 3 ) 912 - 921 2012.9

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DOI： 10.1002/hep.25782

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肥満症におけるGpnmbの意義

片山晶博, 和田淳, 中司敦子, 江口潤, 村上和敏, 神崎資子, 勅使川原早苗, 井上謙太郎, 寺見隆宏, 渡邉真由, 樋口千草, 肥田和之, 四方賢一, 槇野博史

肥満研究 18 ( Suppl. ) 156 - 156 2012.9

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Serum Vaspin Concentrations Are Closely Related to Insulin Resistance, and rs77060950 at SERPINA12 Genetically Defines Distinct Group with Higher Serum Levels in Japanese Population Reviewed

Sanae Teshigawara, Jun Wada, Kazuyuki Hida, Atsuko Nakatsuka, Jun Eguchi, Kazutoshi Murakami, Motoko Kanzaki, Kentaro Inoue, Takahiro Terami, Akihiro Katayama, Izumi Iseda, Yuichi Matsushita, Nobuyuki Miyatake, John F. McDonald, Kikuko Hotta, Hirofumi Makino

JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM 97 ( 7 ) E1202 - E1207 2012.7

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DOI： 10.1210/jc.2011-3297

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RXR antagonism induces G0/G1 cell cycle arrest and ameliorates obesity by up-regulating the p53-p21(Cip1) pathway in adipocytes Reviewed

Atsuko Nakatsuka, Jun Wada, Kazuyuki Hida, Aya Hida, Jun Eguchi, Sanae Teshigawara, Kazutoshi Murakami, Motoko Kanzaki, Kentaro Inoue, Takahiro Terami, Akihiro Katayama, Daisuke Ogawa, Hiroyuki Kagechika, Hirofumi Makino

JOURNAL OF PATHOLOGY 226 ( 5 ) 784 - 795 2012.4

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DOI： 10.1002/path.3001

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Galectin-9 and T Cell Immunoglobulin Mucin-3 Pathway Is a Therapeutic Target for Type 1 Diabetes Reviewed

Motoko Kanzaki, Jun Wada, Koichi Sugiyama, Atsuko Nakatsuka, Sanae Teshigawara, Kazutoshi Murakami, Kentaro Inoue, Takahiro Terami, Akihiro Katayama, Jun Eguchi, Hisaya Akiba, Hideo Yagita, Hirofumi Makino

ENDOCRINOLOGY 153 ( 2 ) 612 - 620 2012.2

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DOI： 10.1210/en.2011-1579

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Telmisartan attenuates diabetic nephropathy by suppressing oxidative stress in db/db mice. Reviewed International journal

Sato-Horiguchi C, Ogawa D, Wada J, Tachibana H, Kodera R, Eguchi J, Nakatsuka A, Terami N, Shikata K, Makino H

Nephron. Experimental nephrology 121 ( 3-4 ) e97 - e108 2012

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BACKGROUND/AIMS: Telmisartan, an angiotensin II type 1 receptor blocker, is widely used to treat hypertension and kidney diseases, including diabetic nephropathy, because of its renoprotective effects. However, the mechanism by which telmisartan prevents proteinuria and renal dysfunction in diabetic nephropathy is still unclear. In this study, we examined the effects of telmisartan against diabetic nephropathy in db/db mice. METHODS: Telmisartan was administered at a dose of 5 mg/kg/day for 3 weeks to db/db (diabetic) and db/m (control) mice. Urinary albumin excretion, renal histology, and the gene expression of oxidative stress and inflammatory markers in renal tissue were determined. To evaluate the effects of telmisartan on reactive oxygen species (ROS) production, superoxide was detected by dihydroethidium (DHE) staining in vivo and in vitro. RESULTS: Telmisartan reduced albuminuria, mesangial matrix expansion, macrophage infiltration, and the expression of ROS markers (NADPH oxidase 4- and 8-hydroxydeoxyguanosine) and inflammatory cytokines (monocyte chemoattractant protein-1, osteopontin, and transforming growth factor-β) in the kidney. DHE staining showed that telmisartan decreased ROS generation in the kidney and in cultured mesangial and proximal tubular epithelial cells. CONCLUSIONS: Taken together, these findings indicate that telmisartan protects against diabetic nephropathy by reducing diabetes-induced oxidative stress.

DOI： 10.1159/000343102

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A Case of Type 2 Diabetes and Metastatic Liver Cancer Exhibiting Hypercholesterolemia with Abnormal Lipoproteins Reviewed

Motoko Kanzaki, Jun Wada, Atsuko Nakatsuka, Sanae Teshigawara, Kazutoshi Murakami, Kentaro Inoue, Takahiro Terami, Akihiro Katayama, Junichiro Nasu, Kazuhide Yamamoto, Hirofumi Makino

INTERNAL MEDICINE 51 ( 6 ) 619 - 623 2012

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DOI： 10.2169/internalmedicine.51.6486

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Telmisartan Attenuates Diabetic Nephropathy by Suppressing Oxidative Stress in db/db Mice Reviewed

Chikage Sato-Horiguchi, Daisuke Ogawa, Jun Wada, Hiromi Tachibana, Ryo Kodera, Jun Eguchi, Atsuko Nakatsuka, Naoto Terami, Kenichi Shikata, Hirofumi Makino

NEPHRON EXPERIMENTAL NEPHROLOGY 121 ( 3-4 ) E97 - E108 2012

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DOI： 10.1159/000343102

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Two novel mutations of lecithin:cholesterol acyltransferase (LCAT) gene and the influence of APOE genotypes on clinical manifestations Reviewed

Akihiro Katayama, Jun Wada, Hitomi Usui Kataoka, Hiroko Yamasaki, Sanae Teshigawara, Takahiro Terami, Kentaro Inoue, Motoko Kanzaki, Kazutoshi Murakami, Atsuko Nakatsuka, Hitoshi Sugiyama, Norio Koide, Hideaki Bujo, Hirofumi Makino

NDT Plus 4 ( 5 ) 299 - 302 2011.10

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DOI： 10.1093/ndtplus/sfr091

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[Obesity: Progress in diagnosis and treatment; Topics, IV. Recent topics: 3. Obesity and new secretory factors; 1) Vaspin]. Reviewed

Wada J, Teshigawara S, Nakatsuka A, Makino H

Nihon Naika Gakkai zasshi. The Journal of the Japanese Society of Internal Medicine 100 ( 4 ) 996 - 1001 2011.4

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DOI： 10.2169/naika.100.996

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新規脂肪細胞膜蛋白Gpnmbの同定

片山晶博, 和田淳, 中司敦子, 村上和敏, 神崎資子, 勅使川原早苗, 井上謙太郎, 寺見隆宏, 肥田和之, 四方賢一, 槇野博史

糖尿病 54 ( Suppl.1 ) S - 356 2011.4

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ACAMの脂肪分化とメタボリックシンドロームにおける意義

村上和敏, 和田淳, 中司敦子, 神崎資子, 勅使川原早苗, 寺見隆宏, 井上謙太郎, 片山晶博, 四方賢一, 槇野博史

糖尿病 54 ( Suppl.1 ) S - 132 2011.4

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糖尿病性腎症の糖鎖プロファイングの検討

井上謙太郎, 和田淳, 中司敦子, 村上和敏, 神崎資子, 寺見隆宏, 勅使川原早苗, 黒瀬祐子, 片山晶博, 小川智央, 山田雅雄, 四方賢一, 槇野博史

糖尿病 54 ( Suppl.1 ) S - 225 2011.4

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[Chemerin, RBP4 and vaspin]. Reviewed

Wada J, Teshigawara S, Nakatsuka A

Nihon rinsho. Japanese journal of clinical medicine 69 Suppl 1 231 - 236 2011.1

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メタボリック症候群・慢性腎臓病の核内受容体をターゲットとした治療

中司敦子, 和田淳, 影近弘之, 肥田和之, 村上和敏, 神崎資子, 勅使川原早苗, 寺見隆宏, 井上謙太郎, 小川大輔, 四方賢一, 槇野博史

日本腎臓学会誌 52 ( 3 ) 321 - 321 2010.5

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メタボリック症候群・慢性腎臓病の核内受容体をターゲットとした治療

和田淳, 中司敦子, 影近弘之, 肥田和之, 村上和敏, 神崎資子, 勅使川原早苗, 寺見隆宏, 井上謙太郎, 小川大輔, 四方賢一, 槇野博史

糖尿病 53 ( Suppl.1 ) S - 251 2010.4

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ACAMの脂肪分化とメタボリックシンドロームにおける意義

村上和敏, 和田淳, 中司敦子, 勅使川原早苗, 神崎資子, 吉川理津子, 寺見隆宏, 井上謙太郎, 黒瀬祐子, 四方賢一, 槇野博史

糖尿病 52 ( Suppl.1 ) S - 162 2009.4

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ヒト血中Vaspin濃度の検討とメタボリックシンドロームにおける意義

勅使川原早苗, 和田淳, 中司敦子, 村上和敏, 神崎資子, 肥田和之, 伊勢田泉, 利根淳仁, 松下裕一, 宮武伸行, 井上謙太郎, 寺見隆宏, 黒瀬裕子, 四方賢一, 槇野博史

糖尿病 52 ( Suppl.1 ) S - 245 2009.4

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RXRアンタゴニストによる細胞周期異常制御とメタボリック症候群

中司敦子, 和田淳, 村上和敏, 神崎資子, 勅使川原早苗, 井上謙太郎, 寺見隆宏, 黒瀬祐子, 四方賢一, 影近弘之, 槇野博史

糖尿病 52 ( Suppl.1 ) S - 246 2009.4

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Collectrin Is Involved in the Development of Salt-Sensitive Hypertension by Facilitating the Membrane Trafficking of Apical Membrane Proteins via Interaction With Soluble N-Ethylmaleiamide-Sensitive Factor Attachment Protein Receptor Complex Reviewed

Akihiro Yasuhara, Jun Wada, Sandra M. Malakauskas, Yanling Zhang, Jun Eguchi, Atsuko Nakatsuka, Kazutoshi Murakami, Motoko Kanzaki, Sanae Teshigawara, Kazuya Yamagata, Thu H. Le, Hirofumi Makino

CIRCULATION 118 ( 21 ) 2146 - 2155 2008.11

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DOI： 10.1161/CIRCULATIONAHA.108.787259

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ヒト血中Vaspin濃度の検討とメタボリックシンドロームにおける意義

勅使川原早苗, 和田淳, 中司敦子, 村上和敏, 神崎資子, 寺見隆宏, 井上謙太郎, 肥田和之, 伊勢田泉, 利根淳仁, 松下裕一, 宮武伸行, 四方賢一, 槇野博史

肥満研究 14 ( Suppl. ) 196 - 196 2008.9

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ACAMの脂肪分化とメタボリックシンドロームにおける意義

村上和敏, 和田淳, 中司敦子, 勅使川原早苗, 神崎資子, 寺見隆宏, 井上謙太郎, 四方賢一, 槇野博史

肥満研究 14 ( Suppl. ) 176 - 176 2008.9

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Adipocyte adhesion molecule (ACAM) inhibits adipocyte hypertrophy in obesity

Kazutoshi Murakami, Jun Wada, Atsuko Nakatsuka, Motoko Kanzaki, Sanae Teshigawara, Takahiro Terami, Kentaro Inoue, Hirofumi Makino

DIABETES 57 A110 - A111 2008.6

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Serum vaspin levels correlate with the accumulation of visceral adipose tissues in type 2 diabetes patients

Sanae Teshigawara, Jun Wada, John Mcdonald, Jehangir Mistry, Atsuko Nakatsuka, Kazutoshi Murakami, Motoko Kanzaki, Takahiro Terami, Kentaro Inoue, Hirofumi Makino

DIABETES 57 A394 - A395 2008.6

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Vaspin (visceral adipose tissue-derived serpin), improves insulin sensitivity in metabolic syndrome

Atsuko Nakatsuka, Jun Wada, Kazutoshi Murakami, Sanae Teshigawara, Motoko Kanzaki, Kentaro Inoue, Takahiro Terami, Hirofumi Makino

DIABETES 57 A396 - A396 2008.6

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Galectin-9 inhibits the development of type 1 diabetes in female NOD mice

Motoko Kanzaki, Jun Wada, Atsuko Nakatsuka, Kazutoshi Murakami, Sanae Teshigawara, Takahiro Terami, Kentaro Inoue, Hirofumi Makino

DIABETES 57 A78 - A78 2008.6

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Procollagen C-proteinase enhancer-1 (POPE-1) interacts with beta 2-microglobulin (beta 2-m) and may help initiate beta 2-m amyloid fibril formation in connective tissues Reviewed

Hisanori Morimoto, Jun Wada, Bernard Font, Joni D. Mott, David J. S. Hulmes, Tadakazu Ookoshi, Hironobu Naiki, Akihiro Yasuhara, Atsuko Nakatsuka, Kousuke Fukuoka, Yuji Takatori, Haruo Ichikawa, Shigeru Akagi, Kazushi Nakao, Hirofumi Makino

MATRIX BIOLOGY 27 ( 3 ) 211 - 219 2008.4

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DOI： 10.1016/j.matbio.2007.11.005

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ヒト血中Vaspin濃度の検討とメタボリックシンドロームにおける意義

勅使川原早苗, 和田淳, 中司敦子, 村上和敏, 肥田和之, 伊勢田泉, 利根淳仁, 松下裕一, 宮武伸行, 井上謙太郎, 寺見隆宏, 四方賢一, 槇野博史

糖尿病 51 ( Suppl.1 ) S - 308 2008.4

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Galectin-9による1型糖尿病発症抑制の検討

神崎資子, 和田淳, 吉川理津子, 中司敦子, 村上和敏, 安原章浩, 勅使川原早苗, 井上謙太郎, 寺見隆宏, 四方賢一, 槇野博史

糖尿病 51 ( Suppl.1 ) S - 211 2008.4

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ACAMの脂肪分化とメタボリックシンドロームにおける意義

村上和敏, 和田淳, 中司敦子, 神崎資子, 安原章浩, 吉川理津子, 勅使川原早苗, 井上謙太郎, 寺見隆宏, 四方賢一, 槇野博史

糖尿病 51 ( Suppl.1 ) S - 306 2008.4

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Vaspinのメタボリックシンドロームにおける意義

中司敦子, 和田淳, 村上和敏, 神崎資子, 安原章浩, 吉川理津子, 勅使川原早苗, 井上謙太郎, 寺見隆宏, 四方賢一, 槇野博史

糖尿病 51 ( Suppl.1 ) S - 307 2008.4

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Adipocyte adhesion molecule (ACAM) inhibits adipocyte hypertrophy in obesity

K. Murakami, J. Wada, A. Nakatsuka, S. Teshigawara, R. Yoshikawa, M. Kanzaki, A. Yasuhara, K. Shikata, H. Makino

DIABETOLOGIA 50 S57 - S57 2007.9

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Vaspin improves insulin sensitivity in obesity

A. Nakatsuka, J. Wada, K. Murakami, S. Teshigawara, R. Yoshikawa, M. Kanzaki, A. Yasuhara, K. Shikata, H. Makino

DIABETOLOGIA 50 S56 - S56 2007.9

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脂肪細胞分化 ACAMトランスジェニックマウスとメタボリック症候群

村上和敏, 和田淳, 中司敦子, 神崎資子, 勅使川原早苗, 四方賢一, 槇野博史

肥満研究 13 ( Suppl. ) 157 - 157 2007.9

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Vaspinとメタボリック症候群

中司敦子, 和田淳, 村上和敏, 神崎資子, 勅使川原早苗, 四方賢一, 槇野博史

肥満研究 13 ( Suppl. ) 193 - 193 2007.9

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Vaspin(visceral adipose tissue-derived serpin)とインスリン抵抗性

中司敦子, 和田淳, 村上和敏, 勅使川原早苗, 吉川理津子, 神崎資子, 四方賢一, 槇野博史

糖尿病 50 ( Suppl.1 ) S - 166 2007.4

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Adipocyte adhesion molecule(ACAM)トランスジェニックマウスとメタボリックシンドローム

村上和敏, 和田淳, 中司敦子, 勅使川原早苗, 吉川理津子, 神崎資子, 安原章浩, 四方賢一, 槇野博史

糖尿病 50 ( Suppl.1 ) S - 163 2007.4

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Hemophagocytic syndrome associated with fatal veno-occlusive disease in the liver Reviewed

Atsuko Nakatsuka, Jun Wada, Ryo Nagase, Masaya Takeda, Tadashi Yoshino, Hirofumi Makino

INTERNAL MEDICINE 46 ( 8 ) 495 - 499 2007

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DOI： 10.2169/internalmedicine.46.6294

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[Molecular biology of regulation in renal functions; biosynthesis, metabolism, and action of insulin and glucagon]. Reviewed

Nakatsuka A, Wada J, Makino H

Nihon rinsho. Japanese journal of clinical medicine 64 Suppl 2 222 - 226 2006.2

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Visceral adipose tissue-derived serine protease inhibitor: A unique insulin-sensitizing adipocytokine in obesity Reviewed

K Hida, J Wada, J Eguchi, H Zhang, M Baba, A Seida, L Hashimoto, T Okada, A Yasuhara, A Nakatsuka, K Shikata, S Hourai, J Futami, E Watanabe, Y Matsuki, R Hiramatsu, S Akagi, H Makino, YS Kanwar

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 102 ( 30 ) 10610 - 10615 2005.7

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DOI： 10.1073/pnas.0504703102

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A case of monoclonal immunoglobulin light- and heavy-chain deposition disease exhibting atypical deposition with fibrillary structures, successfully treated with chemotherapy Reviewed

NAKATSUKA A

Clin Nephrol 64 221 - 227 2005

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VASPIN(visceral adipose tissue specific SERPIN)とインスリン抵抗性

肥田和之, 和田淳, 江口潤, 松岡孝至, 橋本泉, 安原章浩, 中司敦子, 清田綾, 岡田達夫, 馬場雅子, 四方賢一, 槇野博史

糖尿病 47 ( Suppl.1 ) S252 - S252 2004.4

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糖尿病性腎症に対するPioglitazoneの作用メカニズムの検討

岡田達夫, 和田淳, 肥田和之, 江口潤, 橋本泉, 馬場雅子, 松岡孝至, 安原章浩, 清田綾, 中司敦子, 四方賢一, 槇野博史

糖尿病 47 ( Suppl.1 ) S195 - S195 2004.4

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白色脂肪特異的新規膜蛋白(OL-16)の機能解析

江口潤, 和田淳, 肥田和之, 松岡孝至, 馬場雅子, 中司敦子, 橋本泉, 清田綾, 安原章浩, 岡田達夫, 四方賢一, 槇野博史

肥満研究 9 ( Suppl. ) 76 - 76 2003.10

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A case of focal segmental glomerulosclerosis (FSGS) complicated with chronic hepatitis B and treated with steroid and LDL apheresis Reviewed

Akinobu Takaki, Atsuko Nakatsuka, Chikage Satou, Yasuyoshi Iwata, Hiroshi Ikeda, Masaki Fukushima

Japanese Journal of Nephrology 44 ( 8 ) 806 - 812 2002

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糖尿病と心腎連関

中司敦子, 和田淳

循環器内科 90 ( 6 ) 601 - 609 2021.12

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DKDの基礎小胞体ストレス（特集糖尿病性腎臓病DKD)

中司敦子, 和田淳

腎と透析 91 ( 4 ) 568 - 574 2021.10

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バスピンとメタボリックシンドローム

和田淳, 中司敦子, 江口潤

日本動脈硬化学会総会・学術集会プログラム・抄録集(Web) 52nd 2020

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尿細管間質障害におけるHSPA1Lの意義

中司敦子, 江口潤, 和田淳

日本腎臓学会誌(Web) 62 ( 4 ) 2020

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脂肪肝における脂肪酸20:3(n6),20:3(n9)の意義

中司敦子, 山口哲志, 江口潤, 和田淳

糖尿病(Web) 62 ( Suppl ) 2019

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糖尿病における近位尿細管細胞のGRP78局在変化とバスピンの受容体としての意義

中司敦子, 江口潤, 和田淳

日本腎臓学会誌 61 ( 3 ) 2019

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肥満糖尿病の近位尿細管障害におけるHSPsの新規作用機序の解明

中司敦子, 山口哲志, 江口潤, 和田淳

日本肥満学会・日本肥満症治療学会合同学術集会プログラム・抄録集 40th-37th 2019

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肥満・糖尿病の近位尿細管障害に対する分子シャペロンの新規機能の解明

中司敦子, 山口哲志, 高橋寛子, 柴田祐助, 勅使川原早苗, 江口潤, 和田淳

糖尿病(Web) 61 ( Suppl ) 2018

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肥満症関連腎臓病とDKDの接点

和田淳, 中司敦子, 三瀬広記, 江口潤

肥満研究 24 ( Supplement ) 2018

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肥満糖尿病における尿細管障害とHSPsを介したvapsinの作用機序の解明

中司敦子, 山口哲志, 江口潤, 和田淳

肥満研究 24 ( Supplement ) 2018

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糖尿病性腎症の基礎研究（特集糖尿病性腎症）

中司敦子, 和田淳

日本腎臓学会誌 59 ( 2 ) 58 - 64 2017.2

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糖尿病と心腎連関（特集心腎連関を理解する）

中司敦子, 和田淳

臨床検査 62 72 - 77 2017.1

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肥満・糖尿病による近位尿細管細胞障害とvaspinの細胞保護作用機序の解明

中司敦子, 山口哲志, 柴田祐助, 高橋寛子, 三瀬広記, 勅使川原早苗, 江口潤, 和田淳

糖尿病(Web) 60 ( Suppl ) 2017

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肥満症と腎疾患

和田淳, 中司敦子, 江口潤

肥満研究 23 ( Supplement ) 2017

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肥満・糖尿病における近位尿細管細胞障害とアディポカインvaspinの作用

中司敦子, 江口潤, 和田淳

日本腎臓学会誌 59 ( 3 ) 2017

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メタボリックシンドロームにおける尿細管障害機構の解明とvaspinの細胞保護作用

中司敦子, 山口哲志, 高橋寛子, 柴田祐助, 勅使川原早苗, 江口潤, 和田淳

肥満研究 23 ( Supplement ) 2017

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血糖制御に関わる臓器・関連因子－脂肪細胞

中司敦子, 和田淳

日本臨牀. 増刊号 ( 1 ) 258 - 262 2016.1

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Vaspinの肥満症における腎障害抑制機序の解明

中司敦子, 山口哲志, 柴田祐助, 勅使川原早苗, 江口潤, 和田淳

肥満研究 22 ( Supplement ) 2016

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糖尿病腎症におけるvaspinの意義

中司敦子, 山口哲士, 柴田祐助, 勅使川原早苗, 江口潤, 和田淳

糖尿病(Web) 59 ( Suppl ) 2016

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【最新エビデンスに学ぶ効果の上がる肥満症食事療法の実践】肥満に起因する各種疾患の診療肥満関連腎臓病

中司敦子, 和田淳

臨床栄養 127 ( 4 ) 441 - 444 2015.9

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【腎臓とエネルギー代謝】肥満関連腎症

和田淳, 中司敦子, 北川正史

腎臓内科・泌尿器科 2 ( 2 ) 138 - 142 2015.8

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肥満と腎障害 (特集肥満に伴う臓器障害) -- (肥満に伴う臓器障害の成因と病態)

中司敦子, 和田淳

ホルモンと臨床 63 ( 2 ) 103 - 107 2015.2

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Vaspinのメタボリックシンドロームにおける意義

和田淳, 中司敦子, 槇野博史

腎と透析 78 267 - 271 2015.2

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慢性腎臓病(CKD) (特集肥満症診療最前線) -- (肥満に起因する疾患の検査,治療のポイントは? : 体重減少の効果を主に）

中司敦子, 和田淳

Modern Physician. 35 ( 2 ) 216 - 218 2015.2

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【代謝異常による腎疾患の発症機序解明と治療法開発】Vaspinのメタボリックシンドロームにおける意義

和田淳, 中司敦子, 槇野博史

腎と透析 78 ( 2 ) 267 - 271 2015.2

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Vaspin

77 ( 6 ) 569 - 574 2015

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糖尿病腎症の分子機構と診断・治療への展開

和田淳, 中司敦子, 江口潤

糖尿病学の進歩 49th 2015

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肥満関連腎症におけるvaspinの意義

中司敦子, 村上和敏, 勅使川原早苗, 山口哲志, 柴田祐助, 天田雅文, 片山晶博, 江口潤, 和田淳

肥満研究 21 ( Supplement ) 2015

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メタボリックシンドロームにおけるphosphatidylethanolamine N-methyltransferase(PEMT)が関与する脂肪肝炎と肝再生機構

中司敦子, 村上和敏, 勅使川原早苗, 片山晶博, 天田雅文, 布上朋和, 山口哲志, 江口潤, 小川大輔, 和田淳

糖尿病 58 ( Supplement 1 ) 2015

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肥満症と腎疾患

和田淳, 中司敦子, 勅使川原早苗, 村上和敏, 江口潤

肥満研究 21 ( Supplement ) 2015

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【肥満の医学-臨床と研究の最先端】基礎研究【脂肪細胞のKey Molecules】Vaspin

中司敦子, 和田淳

医学のあゆみ 250 ( 9 ) 837 - 838 2014.8

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糖尿病血管合併症におけるVaspinの意義の解明

中司敦子, 和田淳, 槇野博史

糖尿病合併症 28 ( 2 ) 148 - 154 2014.6

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メタボリックシンドロームに伴う脂肪肝炎とPemtの意義

中司敦子, 村上和敏, 勅使川原早苗, 片山晶博, 布上朋和, 天田雅文, 山口哲志, 江口潤, 和田淳

肥満研究 20 ( Supplement ) 2014

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Vaspin and insulin resistance

37 ( 6 ) 633 - 639 2013.12

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Vaspinによる小胞体ストレス制御と糖尿病性腎症の治療

中司敦子, 和田淳, 勅使川原早苗, 井上謙太郎, 寺見隆宏, 片山晶博, 村上和敏, 江口潤, 小川大輔, 槇野博史

日本腎臓学会誌 55 ( 3 ) 2013

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糖尿病性腎症におけるPEMT阻害の意義

中司敦子, 和田淳, 渡辺真由, 勅使川原早苗, 村上和敏, 井上謙太郎, 寺見隆宏, 片山晶博, 江口潤, 小川大輔, 槇野博史

日本腎臓学会誌 55 ( 3 ) 2013

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メタボリックシンドロームにおけるphosphatidylethanolamine N-methyltransferase(PEMT)の意義

中司敦子, 和田淳, 村上和敏, 勅使川原早苗, 井上謙太郎, 寺見隆宏, 片山晶博, 渡邉真由, 樋口千草, 江口潤, 小川大輔, 槇野博史

糖尿病 56 ( Supplement 1 ) 2013

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肥満においてPemt欠損がもたらす脂肪肝炎とエピゲノム

中司敦子, 和田淳, 渡邊真由, 樋口千草, 天田雅文, 布上朋和, 片山晶博, 寺見隆宏, 勅使川原早苗, 村上和敏, 江口潤, 槇野博史

肥満研究 19 ( Supplement ) 2013

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糖尿病性腎症の糖鎖プロファイリングによる新規バイオマーカーの同定(U-CARE研究)

和田淳, 井上謙太郎, 中司敦子, 江口潤, 村上和敏, 寺見隆宏, 勅使川原早苗, 片山晶博, 小川智央, 山田雅雄, 四方賢一, 槇野博史

日本腎臓学会誌 55 ( 3 ) 2013

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RXR antagonism induces G0/G1 cell cycle arrest and ameliorates obesity by up-regulating p53-p21^Cip1 pathway in adipocytes

124 ( 2 ) 97 - 100 2012.8

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DOI： 10.4044/joma.124.97

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ヒト血中Vaspin濃度の検討とメタボリックシンドロームにおける意義

勅使川原, 早苗, 和田淳, 中司敦子, 堀田紀久子, 肥田和之, 村上和敏, 神崎資子, 井上謙太郎, 寺見隆宏, 松下裕一, 片山晶博, 江口潤, 槇野博史

肥満研究 17 ( Suppl. ) 160 - 160 2011.9

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Vaspin and insulin resistance in metabolic syndrome

66 ( 6 ) 599 - 604 2011.6

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【メタボリックシンドローム(第2版) 基礎・臨床の最新知見】成因と病態生理メタボリックシンドローム発症基盤としての脂肪細胞機能異常アディポサイトカインとその役割ケマリン、レチノール結合タンパク(RBP4)、バスピン

和田淳, 勅使川原早苗, 中司敦子

日本臨床 69 ( 増刊1 メタボリックシンドローム ) 231 - 236 2011.1

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メタボリックシンドロームにおけるphosphatidylethanolamine N-methyltransferase(PEMT)の意義

中司敦子, 和田淳, 村上和敏, 神崎資子, 勅使川原早苗, 寺見隆宏, 井上謙太郎, 片山晶博, 四方賢一, 槇野博史

糖尿病 54 ( Supplement 1 ) 2011

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腎症における細胞周期異常と核内受容体をターゲットとした治療

中司敦子, 和田淳, 村上和敏, 神崎資子, 勅使川原早苗, 四方賢一, 槇野博史

Diabetes Frontier 21 ( 5 ) 626 - 627 2010.10

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ヒト血中Vaspin濃度の検討とメタボリックシンドロームにおける意義

勅使川原, 早苗, 和田淳, 中司敦子, 村上和敏, 神崎資子, 井上謙太郎, 寺見隆宏, 松下裕一, 利根淳仁, 伊勢田泉, 肥田和之, 宮武伸行, 堀田紀久子, 四方賢一, 槇野博史

糖尿病 53 ( Suppl.1 ) S - 164 2010.4

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【脂質代謝異常と腎臓の接点】チアゾリジン誘導体による腎保護効果

中司敦子, 和田淳, 槇野博史

The Lipid 21 ( 2 ) 159 - 166 2010.4

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Vaspinによる炎症制御とインスリン抵抗性

中司敦子、和田淳

医学のあゆみ 229 ( 7 ) 526 - 530 2009.5

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DEBATE 尿所見と心血管事故糖尿病の立場から

中司敦子, 和田淳, 槇野博史

臨床高血圧 12 ( 2 ) 116 - 122 2006.6

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【分子腎臓病学分子生物学的アプローチと分子病態生理学】基礎編腎機能調節におけるホルモンおよびペプチドの分子生物学生合成,代謝,作用インスリン/グルカゴン

中司敦子, 和田淳, 槇野博史

日本臨床 64 ( 増刊2 分子腎臓病学 ) 222 - 226 2006.2

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Vaspin(visceral Adipose Tissue-derived Serine Protease Inhibitor)とインスリン抵抗性

中司敦子, 和田淳, 村上和敏, 肥田和之, 肥田綾, 江口潤, 江口雅子, 伊勢田泉, 安原章浩, 岡田達夫, 四方賢一, 槙野博史

糖尿病 49 ( Supplement 1 ) 2006

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Relationship between the length of the predialysis period and the pathogenesis of diabetic end-stage renal failure

Nakatsuka Atsuko, Kanzaki Motoko, Iwata Yasuyoshi, Takaki Akinobu, Ikeda Hiroshi, Fukushima Masaki

Journal of Japanese Society for Dialysis Therapy 38 ( 8 ) 1385 - 1390 2005

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To examine the relationship between the length of the predialysis period and the pathogenesis of diabetic end-stage renal failure, we retrospectively studied 58 hemodialyzed patients (36 males, 22 females; 62.8±10.6 (SD) years). They were subgrouped into group A (n=34) or B (n=29), respectively, depending on whether hemodialysis was started less or more than 2 years after their serum creatinine concentration had reached 2mg/dL. Group A patients were ten years younger than those of group B, and showed significantly higher urinary protein excretion, lower plasma albumin concentration, and larger renal size. The incidence of cerebral infarction was higher in group B. Multiple regression analysis demonstrated that the length of predialysis period was well correlated with both patients' age and renal size. These findings suggest that the major pathogenesis of renal failure is microangiopathic glomerulosclerosis in group A, and macroangiopathic nephrosclerosis in group B. The length of the predialysis period in each case must reflect the different involvements of these two mechanisums. Especially, in older hemodialyzed diabetic patients, the number of which has been increasing in recent years, nephrosclerosis may play a larger role in diabetic nephropathy.

DOI： 10.4009/jsdt.38.1385

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Consciousness disturbance due to hypermagnesemia in two patients with chronic renal failure

Nakatsuka Atsuko, Kanzaki Motoko, Takaki Akinobu, Iwata Yasuyoshi, Ikeda Hiroshi, Fukushima Masaki

Journal of Japanese Society for Dialysis Therapy 37 ( 2 ) 163 - 168 2004

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Consciousness disturbances in untreated end stage renal failure are referred to as uremic encephalopathy, which is now rare in Japan as dialysis therapy is readily available. We describe two chronic renal failure (CRF) patients who developed consciousness disturbances attributable to hypermagnesemia. Case 1. A 77-year-old man with CRF due to diabetic nephropathy was transferred to our hospital because of appetite loss and drowsiness. Serum creatinine and blood urea nitrogen (BUN) levels were 4.31 and 64mg/dL, respectively. The serum magnesium (Mg) level was found to be as high as 7.3mg/dL. The calcium level was 5.8mg/dL. He had cutaneous flushing and respiratory insufficiency caused by respiratory depression in addition to pneumonia. The serum Mg level decreased after hemodialysis with improvement of consciousness disturbances. However, the serum Mg level rose again on the next day, and an additional hemodialysis session was needed. Case 2. A 78-year-old woman with rheumatoid arthritis developed urinary tract infection which induced acute deterioration of CRF. She demonstrated general fatigue and disorientation. The serum Mg, creatinine and BUN levels were 7.1, 6.56 and 96mg/dL, respectively. Her consciousness level was normalized as the Mg levels decreased after three successive days of hemodialysis. Both of these patients demonstrated rather mild azotemia and developed consciousness disturbances during the use of magnesium oxide. Of our 78 patients starting hemodialysis in the past two years, only these two patients demonstrated toxic serum Mg levels. We suggest that the use of Mg can cause symptomatic hypermagnesemia in patients with acute deterioration of CRF, and that hypocalcemia may worsen the manifestations of hypermagnesemia. Conclusions: As Mg toxicity is a serious and potentially fatal condition, early and accurate diagnosis must be made especially in CRF patients with consciousness disturbances. Hemodialysis is effective for the treatment, but postdialysis rebound of the serum Mg level must be carefully observed.

DOI： 10.4009/jsdt.37.163

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糖尿病性腎症に合併したANCA関連急速進行性糸球体腎炎の1例

中司敦子, 佐藤千景, 岩田康義, 高木章乃夫, 福島正樹, 津嘉山朝達, 西崎哲一

腎と透析 2002

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アンギオテンシン変換酵素阻害剤(ACE-I)投与中に発生した急性腎不全症例の検討

高木章乃夫, 岩田康義, 佐藤千景, 江口潤, 中司敦子, 福島正樹

ICUとCCU 26 S150 - 152 2002

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慢性B型肝炎に巣状分節性糸球体硬化症(FSGS)によるネフローゼ症候群を合併し,ステロイド,LDL吸着療法にて緩解した1例

高木章乃夫, 央病院, 腎臓内科, 中司敦子, 佐藤千景, 岩田康義, 池田弘, 福島正樹

日本腎臓学会誌 2002

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DOI： 10.14842/jpnjnephrol1959.44.806

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ANCA関連腎炎の治療と予後に関する検討

中司敦子, 高木章乃夫, 岩田康義, 福島正樹

倉敷中央病院年報 2002

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深部静脈血栓症（DVT)を合併した糖尿病性腎症透析患者の一例

山崎浩子, 長宅芳男, 平櫛恵太, 肥田和之, 中司敦子, 西下伸吾, 大石和弘, 福田真治, 槇野博史, 万波智彦, 吉野正, 赤木忠厚

中国腎不全研究会誌 1999

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Presentations

オルガネラに注目した肥満・糖尿病における近位尿細管障害とVaspin研究の展開 Invited

中司敦子

第45回日本肥満学会 2024.10.20

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Event date： 2024.10.19 - 2024.10.20

Language：Japanese Presentation type：Symposium, workshop panel (nominated)

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肥満症・糖尿病におけるVaspin研究の展開 Invited

中司敦子

第39回糖尿病合併症学会 2024.10.4

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Event date： 2024.10.4 - 2024.10.5

Language：Japanese Presentation type：Symposium, workshop panel (nominated)

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Vaspin/HSPA1L経路を介したミトコンドリア機能維持と尿細管間質障害の抑制

中司敦子, 神野文香, 和田淳

第67回日本糖尿病学会年次学術集会 2024.5.17

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Event date： 2024.5.17 - 2024.5.19

Language：Japanese Presentation type：Oral presentation (general)

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Significance of Vaspin in Metabolic Syndrome and Perspectives Invited

Atsuko Nakatsuka

2024.3.8

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Event date： 2024.3.8 - 2024.3.9

Language：Japanese Presentation type：Oral presentation (invited, special)

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DKDにおけるVaspin/GRP78研究の展開 Invited

中司敦子

第65回日本腎臓学会総会 2022.6.10

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Event date： 2022.6.12

Presentation type：Symposium, workshop panel (nominated)

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糖尿病性腎症における細胞表面 GRP78 と vaspin の意義 Invited

中司敦子, 和田淳

第65回日本糖尿病学会総会 2022.5.13

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Event date： 2022.5.12 - 2022.5.13

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アディポカインVaspinを通して考える肥満症の病態形成における腎臓の意義 Invited

中司敦子、和田淳

第42回日本肥満学会 2022.3.26

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Event date： 2022.3.27

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糖尿病における近位尿細管障害とVaspin/HSP70sの意義

中司敦子

第32回日本糖尿病性腎症研究会（ワークショップ） 2021.12.5

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Event date： 2021.12.4 - 2021.12.5

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基礎研究と臨床の間で考える糖尿病合併症（女性医師ワークショップ） Invited

中司敦子

日本糖尿病学会中国四国地方会第59回総会 2021.10.22

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Event date： 2021.10.22 - 2021.10.23

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糖尿病合併症におけるバスピンの作用と新たな病態解明 (女性研究者賞受賞講演） Invited

中司敦子

第64回日本糖尿病学会年次学術集会 2021.5.21

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Event date： 2021.5.20 - 2021.5.22

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臨床医・研究者として継続してきたVaspinの機能解析（会長企画ー研究者のサークルを作ろうー3 女性、連携、新しい糖尿病学を切り拓く）

中司敦子

第64回日本糖尿病学会年次学術集会 2021.5.20

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Event date： 2021.5.20 - 2021.5.22

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肥満糖尿病の近位尿細管障害におけるHSPsの新規機能の解明

中司敦子,山口哲志,江口潤,和田淳

第40回日本肥満学会 2019.11.2

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Event date： 2019.11.2 - 2019.11.3

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糖尿病における近位尿細管細胞のGRP78局在変化とバスピンの受容体としての意義

中司敦子、江口潤、和田淳

第62回日本腎臓学会総会 2019.6.21

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Event date： 2019.6.21 - 2019.6.23

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脂肪肝における脂肪酸20：3（n6），20：3（n9）の意義

中司敦子, 山口哲志, 江口潤, 和田淳

第62回日本糖尿病学会年次学術集会 2019.5.24

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Event date： 2019.5.23 - 2019.6.25

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肥満症関連腎臓病とDKDの接点

和田淳, 中司敦子, 三瀬広記, 江口潤

肥満研究 2018

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Event date： 2018

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肥満糖尿病における尿細管障害とHSPsを介したvapsinの作用機序の解明

中司敦子, 山口哲志, 江口潤, 和田淳

肥満研究 2018

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Event date： 2018

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肥満・糖尿病の近位尿細管障害に対する分子シャペロンの新規機能の解明

中司敦子, 山口哲志, 高橋寛子, 柴田祐助, 勅使川原早苗, 江口潤, 和田淳

糖尿病(Web) 2018

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Event date： 2018

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肥満症と腎疾患

和田淳, 中司敦子, 江口潤

肥満研究 2017

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Event date： 2017

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肥満・糖尿病における近位尿細管細胞障害とアディポカインvaspinの作用

中司敦子, 江口潤, 和田淳

日本腎臓学会誌 2017

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Event date： 2017

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メタボリックシンドロームにおける尿細管障害機構の解明とvaspinの細胞保護作用

中司敦子, 山口哲志, 高橋寛子, 柴田祐助, 勅使川原早苗, 江口潤, 和田淳

肥満研究 2017

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Event date： 2017

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肥満関連腎症におけるvaspinの意義

中司敦子, 村上和敏, 勅使川原早苗, 山口哲志, 柴田祐助, 天田雅文, 片山晶博, 江口潤, 和田淳

肥満研究 2015

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Event date： 2015

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メタボリックシンドロームにおけるphosphatidylethanolamine N-methyltransferase(PEMT)が関与する脂肪肝炎と肝再生機構

中司敦子, 村上和敏, 勅使川原早苗, 片山晶博, 天田雅文, 布上朋和, 山口哲志, 江口潤, 小川大輔, 和田淳

糖尿病 2015

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Event date： 2015

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肥満症と腎疾患

和田淳, 中司敦子, 勅使川原早苗, 村上和敏, 江口潤

肥満研究 2015

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Event date： 2015

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メタボリックシンドロームに伴う脂肪肝炎とPemtの意義

中司敦子, 村上和敏, 勅使川原早苗, 片山晶博, 布上朋和, 天田雅文, 山口哲志, 江口潤, 和田淳

肥満研究 2014

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Event date： 2014

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糖尿病性腎症におけるPEMT阻害の意義

中司敦子, 和田淳, 渡辺真由, 勅使川原早苗, 村上和敏, 井上謙太郎, 寺見隆宏, 片山晶博, 江口潤, 小川大輔, 槇野博史

日本腎臓学会誌 2013

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Event date： 2013

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メタボリックシンドロームにおけるphosphatidylethanolamine N-methyltransferase(PEMT)の意義

中司敦子, 和田淳, 村上和敏, 勅使川原早苗, 井上謙太郎, 寺見隆宏, 片山晶博, 渡邉真由, 樋口千草, 江口潤, 小川大輔, 槇野博史

糖尿病 2013

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肥満においてPemt欠損がもたらす脂肪肝炎とエピゲノム

中司敦子, 和田淳, 渡邊真由, 樋口千草, 天田雅文, 布上朋和, 片山晶博, 寺見隆宏, 勅使川原早苗, 村上和敏, 江口潤, 槇野博史

肥満研究 2013

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糖尿病性腎症の糖鎖プロファイリングによる新規バイオマーカーの同定(U-CARE研究)

和田淳, 井上謙太郎, 中司敦子, 江口潤, 村上和敏, 寺見隆宏, 勅使川原早苗, 片山晶博, 小川智央, 山田雅雄, 四方賢一, 槇野博史

日本腎臓学会誌 2013

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Event date： 2013

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ヒト血中Vaspin濃度の検討とメタボリックシンドロームにおける意義

勅使川原, 早苗, 和田淳, 中司敦子, 堀田紀久子, 肥田和之, 村上和敏, 神崎資子, 井上謙太郎, 寺見隆宏, 松下裕一, 片山晶博, 江口潤, 槇野博史

肥満研究 2011.9 (一社)日本肥満学会

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Event date： 2011.9

Language：Japanese

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ヒト血中Vaspin濃度の検討とメタボリックシンドロームにおける意義

勅使川原, 早苗, 和田淳, 中司敦子, 村上和敏, 神崎資子, 井上謙太郎, 寺見隆宏, 松下裕一, 利根淳仁, 伊勢田泉, 肥田和之, 宮武伸行, 堀田紀久子, 四方賢一, 槇野博史

糖尿病 2010.4 (一社)日本糖尿病学会

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Event date： 2010.4

Language：Japanese

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Vaspin(visceral Adipose Tissue-derived Serine Protease Inhibitor)とインスリン抵抗性

中司敦子, 和田淳, 村上和敏, 肥田和之, 肥田綾, 江口潤, 江口雅子, 伊勢田泉, 安原章浩, 岡田達夫, 四方賢一, 槙野博史

糖尿病 2006

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Homeostasis of Proximal Tubular Cells -Advances in Vaspin/GRP78 Research-

2023.11.30

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Presentation type：Symposium, workshop panel (nominated)

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基礎研究から見えてくるSGLT2阻害薬への期待

中司敦子

日本糖尿病学会中国四国地方会第61回総会シンポジウム1 2023.10.28

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Presentation type：Symposium, workshop panel (nominated)

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糖尿病性腎症における近位尿細管細胞のオルガネラ機能不全

中司敦子

第38回日本糖尿病合併症学会シンポジウム8 2023.10.21

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Presentation type：Symposium, workshop panel (nominated)

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腎症進行予防のためのチーム医療

中司敦子

第57回糖尿病学の進歩 2023.2.18

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Presentation type：Symposium, workshop panel (nominated)

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Vaspin regulates lysosome function and protects from tubulopathy in metabolic syndrome International conference

Nakatsuka Atsuko

Keystone Symposia, Immunometabolism, Metaflammation and Metabolic Disorders (D6) 2019.4

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Language：English Presentation type：Symposium, workshop panel (public)

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Vaspin and proximal tubular cell injury in metabolic syndrome International conference

International Society of Nephrology (ISN) Frontiers Meeting 2018.2

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protective role of vaspin against proximal tubular cell injuries in diabetes mellitus

The 59st Annual Meeting of the Japan Diabetes Society 2016.5

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Awards

岡山市文化奨励賞（学術部門）

2021.11 岡山市

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女性研究者賞

2021.5 日本糖尿病学会

中司敦子

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第2回山﨑倫子賞

2018 日本女医会

中司敦子

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両備檉園記念財団生物学研究奨励賞

2018

中司敦子

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第三内科同門会・奨励賞

2017.12 第三内科同門会

中司敦子
「日本内科学会ことはじめ2017東京」指導教官賞

2017 第114回日本内科学会総会

中司敦子

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ビジョナリーアワード

2016 第37回日本肥満学会

中司敦子

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H27年度研究活動奨励賞

2016 日本女性腎臓病医の会（JSWN

中司敦子

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至誠会賞（旧岡本糸枝賞）

2015

中司敦子

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岡山医学会賞（砂田賞）

2014

中司敦子

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第27回岡本研究奨励賞

2013 公益財団法人成人血管病研究振興財団

中司敦子

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Young Investigator Award

2013 糖尿病合併症学会

中司敦子

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渡辺記念特別奨励賞

2013 宇部興産学術振興財団

中司敦子

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岡山医学会賞（結城賞）

2012

中司敦子

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岡山県医師会学術奨励賞

2012

中司敦子

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第10回日本心臓財団・アステラス・ファイザー「動脈硬化」Update最優秀演題

2012

中司敦子

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優秀演題賞

2010 第54回日本腎臓学会学術大会

中司敦子

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Barrie Hesp scholarship

2010 Keystone symposia

中司敦子

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若手研究奨励賞

2009 第7回メタボリックシンドロームカンファレンス

中司敦子

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優秀演題賞

2009 第52回日本糖尿病学会年次学術集会

中司敦子

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Travel Grant Award

2007 第43回ヨーロッパ糖尿病学会

中司敦子

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第三内科同門会・奨励賞

2005.12 第三内科同門会

中司敦子

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Research Projects

近位尿細管細胞老化とミトコンドリア機能に対するVaspin/HSPA1Lの意義

2022.04 - 2023.03

一般財団法人代謝異常治療研究基金

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Authorship：Principal investigator

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糖尿病腎症の尿細管におけるミトコンドリア過融合とvaspinの意義

2022.04 - 2023.03

日本糖尿病財団・ノボノルディスクファーマ第1回研究助成

中司敦子

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Authorship：Principal investigator

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脂肪肝進行と肝組織修復・再生における特殊脂肪酸の意義

2022.04 - 2023.03

公益財団法人小柳財団 2022年度研究助成金

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ミトコンドリアダイナミクスにおけるバスピンの意義と腎尿細管間質障害の制御

Grant number：20K08608 2020.04 - 2023.03

日本学術振興会科学研究費助成事業基盤研究(C) 基盤研究(C)

中司敦子

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Grant amount：\4420000 （ Direct expense: \3400000 、 Indirect expense：\1020000 ）

我々が同定したアディポカインであるバスピンは肥満糖尿病マウスの近位尿細管細胞に取り込まれて、オルガネラ機能不全を軽減させることを見出した。近位尿細管細胞においてバスピンはGRP78 (78kDa-glucose regulated protein)やHSPA1L（heat shock protein 70kDa-1 like）と結合すること、GRP78およびHSPA1Lはクラスリン重鎖と複合体を形成し、バスピンの細胞内取り込みに関与することが明らかとなった。HSPA1LはHSP70に分類されるが、腎臓における生理的・病態的意義は十分に知られていない。培養近位尿細管細胞(HK2細胞)に10mg/ml bovine serum albumin（BSA）を添加すると、HSPA1Lの培養液への分泌が増加し、細胞内HSPA1L蛋白量は低下し、p62の蓄積が観察された。バスピンはBSAによるHSPA1Lの細胞外分泌を抑制し、p62の蓄積を抑制した。HSPA1Lとlamp2の複合体形成も明らかとなり、バスピンはHSPA1Lを介してオートファジー不全を軽減することが示唆された。
次にストレプトゾトシンで糖尿病を誘発したバスピン欠損マウス(vaspin-/-)の尿細管細胞を電顕で観察すると、玉ねぎ状（多重リング状）に渦巻くミトコンドリアが不均一な分布で観察された。この特徴的なミトコンドリアに着目し、Advanced Bioimaging Support 先端バイオイメージング支援プラットフォームの支援を頂き、SBF-SEM法で立体構築による観察を行った。伸長したミトコンドリアがリング状に彎曲し、さらに外側から包み込むように長いミトコンドリアが彎曲して幾重にも重なる構造が観察でき、割面の場所によって玉ねぎ状に描出された。バスピンのミトコンドリアダイナミクスにおける役割に注目し検討を進めている。

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SGLT2阻害薬によるGRP78を介した尿細管間質障害抑制機構の解明

2020.01 - 2022.01

特定非営利活動法人日本腎臓協会田辺三菱製薬株式会社共同研究

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Authorship：Principal investigator

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キーストンシンポジウム（Molecular & Cellular Biology, Immunometabolism, Metaflammation & Metabolic Disorders）発表

2019

公益財団法人金原一郎記念医学医療振興財団第33回研究交流助成金

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Authorship：Principal investigator

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近位尿細管細胞障害におけるHSPA1Lとオルガネラストレス応答

2018

公益社団法人日本女医会第38回日本女医会学術研究助成

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Authorship：Principal investigator

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シャペロン分子の新規固有機能を介したバスピンの尿細管保護作用の解明と治療への応用

2018

公益財団法人岡山医学振興財団第18回公募助成

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分子シャペロンの新規固有機能と糖尿病腎症における意義の解明

2018

公益財団法人日本糖尿病協会若手研究者助成

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必須脂肪酸欠乏により誘導される生体反応と炎症制御・組織修復への応用

2018

公益財団法人アサヒグループ学術振興財団 2018年度学術研究助成

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肝脂質代謝におけるHeat shock protein 40 Member C1 の機能解析

2018

公益財団法人ノバルティス科学振興財団ノバルティス研究奨励金

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Organelle dysfunction of proximal tubular cells in metabolic syndrome

Grant number：17K09861 2017.04 - 2020.03

Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C) Grant-in-Aid for Scientific Research (C)

Nakatsuka Atsuko

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Grant amount：\4680000 （ Direct expense: \3600000 、 Indirect expense：\1080000 ）

Obesity and diabetes cause proximal tubular cells (PTCs) injury via excessive organelle stresses. In present study, we revealed unique mechanism of PTCs injury induced by palmitate and chemical ER stressor. In HK2 cells, palmitate, tunicamycin and thapsigargin promoted lysosomal membrane permeabilization, leakage of cathepsin B into cytosol, and subsequent NLRP3 inflammasome activation, and ultimately cell death was induced. Vaspin, an adipokine previously we discovered, inhibited this pathway and protected HK2 cells. We newly found that vaspin-interactive molecules, GRP78 and HSPA1L, independently form complex with clathrin heavy chain and both complexes are involved in endocytosis of vaspin. We further identified that intracellular HSPA1L promoted autophagy, and HSPA1L protein level of HK2 cell was decreased by albumin administration accompanied with increased HSPA1L extracellular secretion. Vaspin and HSPA1L may be new therapeutic target to diabetic kidney diseases.

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Dnajc1の新規固有機能の解析と肝脂肪合成における意義

2017

公益財団法人赤枝医学研究財団研究助成

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Authorship：Principal investigator

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オルガネラ機能におけるvaspinの作用と糖尿病腎症の尿細管細胞保護機構の解明

2017

公益財団法人日本糖尿病財団研究助成第4回ベーリンガー/リリー糖尿病研究助成

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Authorship：Principal investigator

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近位尿細管細胞におけるライソゾーム機能異常とvaspinによる細胞保護機構の解明

2016

JSWN研究活動奨励賞

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Authorship：Principal investigator

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アディポカインによる糖尿病性腎症の進展抑制機構の解明－細胞内小器官への作用を中心として-

2016

公益財団法人石橋由紀子記念基金

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Authorship：Principal investigator

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腎尿細管細胞におけるライソゾーム機能の破綻メカニズムの解明

2016

公益財団法人金原一郎記念医学医療振興財団第31回基礎医学研究助成金

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Authorship：Principal investigator

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Vaspinによる近位尿細管細胞の恒常性維持機構の解明

2015 - 2017

公益財団法人持田記念医学薬学振興財団第27回持田記念研究助成金

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Authorship：Principal investigator

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Vaspinによる近位尿細管細胞に対する細胞保護作用の解明

2015

一般社団法人至誠会至誠会賞学術研究助成

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Authorship：Principal investigator

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American Diabetes Association’s 75th Scientific Sessions発表

2015

公益財団法人岡山医学振興会研究交流事業（派遣）助成

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Authorship：Principal investigator

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Vaspin and its interacting molecules as therapeutic targets for metabolic syndrome

Grant number：26293218 2014.04 - 2017.03

Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (B) Grant-in-Aid for Scientific Research (B)

Wada Jun, NAKATSUKA Atsuko

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Grant amount：\16510000 （ Direct expense: \12700000 、 Indirect expense：\3810000 ）

We identified vaspin (visceral adipose tissue-derived serine protease inhibitor) as a novel adlipokine. Vaspin inhibits insulin resistance, fatty liver, dyslipidemia and atherosclerosis in metabolic syndrome. Vaspin inhibits kallikrein 7 belonging to serine protease and increases glucagon-like peptide-1. We generated DNAJC1 (DnaJ homolog, subfamily C, member 1) conditional knockout mice and we demonstrated that they are therapeutic targets for metabolic syndrome.

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The role of vaspin in metabolic syndrome associated renal disease

Grant number：26461361 2014.04 - 2017.03

Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C) Grant-in-Aid for Scientific Research (C)

Nakatsuka Atsuko, WADA Jun

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Grant amount：\4810000 （ Direct expense: \3700000 、 Indirect expense：\1110000 ）

We previously identified an adipokine, vaspin. In this study, we checked the beneficial role of vaspin in renal injury of metabolic syndrome. Vaspin transgenic(Tg) and vaspin-/- mice were fed with high fat high sucrose (HFHS) diet. At 30 weeks of age, prominent vacuolation in the kidney tissues of vaspin-/- mice under HFHS diet are observed, and it is meliorated in Tg mice. These vacuoles are toluidine blue positive and EM demonstrates lysosomal enlargement. TUNEL-positive apoptotic tubular cells increase in vaspin-/- mice fed with HFHS compared with Tg and wild type mice. Next, we investigated the streptozotocin(STZ) induced-diabetes model. In Tg mice, the dilatation and thinning of tubules induced by diabetes are ameliorated. TUNEL-positive apoptotic cells are increased in STZ induced diabetic vaspin-/- mice, while in Tg mice apoptosis was inhibited. It is suspected that vaspin ameliorate tubulointerstitial injury in diabetic and metabolic syndrome associated renal disease.

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The impact of ACAM/CLMP on the adipocytes differentiation and obesity through the primary ciliary machinery

Grant number：26461362 2014.04 - 2017.03

Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C) Grant-in-Aid for Scientific Research (C)

Murakami Kazutoshi, WADA JUN, EGUCHI JUN, NAKATSUKA ATSUKO

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Grant amount：\4810000 （ Direct expense: \3700000 、 Indirect expense：\1110000 ）

The excess of lipid accumulation and hypertrophy of adipocytes induces the abnormality of secretion of adipokines and hormones from adipocytes and causes metabolic syndrome and diabetes. We identified ACAM in 2005 from the visceral fat tissue of obese rats. It is a cell adhesion molecule responsible for the homophilic adhesion of the cells. In the transgemic mice overexpressing ACAM in adipocytes fed with a high fat and high sucrose diet were protected from the onset of obesity and diabetes. In transgemnic mice, ACAM is abundantly expressed on plasma membrane of mature adipocytes and associated with formation of Phalloidin-positive polymerized form of cortical actin (F-actin). By electron microscopy, the structure of zonula adherens was formed at interphase of adipocytes. The adhesion of adipocytes and formation of cortical actin prevent the adipocyte hypertrophy and development of obesity and diabetes.

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Pemt欠損による肝細胞アポトーシス遷延と脂肪肝炎進展機構の解明

2014

公益財団法人山陽放送学術文化財団第52回（平成26年度）学術奨励賞

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Authorship：Principal investigator

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脂肪肝炎における肝再生機構に寄与する脂肪酸の同定

2014

公益財団法人ウイルス肝炎研究財団平成26年度研究奨励金

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Authorship：Principal investigator

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VaspinのGLP-1を介した血糖調節機構の解明

2014

公益財団法人日本糖尿病財団第4回(平成26年度)リリー・インクレチン基礎研究助成金

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Authorship：Principal investigator

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第73回アメリカ糖尿病学会参加・発表, PEMTのメタボリックシンドロームにおける意義の解明

2013

公益財団法人ウエスコ学術振興財団平成25年度学術研究費助成金（海外渡航費助成）

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Authorship：Principal investigator

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糖尿病細小血管障害におけるVaspinの意義

2013

公益財団法人万有生命科学振興国際交流財団 Banyu Foundation Research Grant 2013

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Authorship：Principal investigator

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Vaspinによる小胞体ストレス制御と糖尿病性腎症治療薬の開発

2013

公益財団法人宇部興産学術振興財団第53回学術研究費援助金（渡辺記念特別奨励賞）

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Authorship：Principal investigator

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VDAC/GRP78経路を介した血管内皮細胞アポトーシスの制御

2013

公益財団法人成人血管病研究振興財団平成25年度岡本研究奨励賞

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Authorship：Principal investigator

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The beneficial role of vaspin in metabolic syndrome by amelioration of ER stress

Grant number：24790926 2012.04 - 2014.03

Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research Grant-in-Aid for Young Scientists (B) Grant-in-Aid for Young Scientists (B)

NAKATSUKA Atsuko

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Grant amount：\4160000 （ Direct expense: \3200000 、 Indirect expense：\960000 ）

To study the role of vaspin, we generated vaspin transgenic (Tg) mice and vaspin knockout (KO) mice. Under high fat-high sucrose diet, the obesity, insulin resistance and fatty liver were ameliorated in Tg mice, while they were exacerbated in KO mice. We identified GRP78 as a vaspin-interacting molecule, and GRP78 forms complex with anchor proteins on the plasma membrane. On hepatocytes, vaspin interacts with GRP78/MTJ-1 complex and enhance the phosphorylation of Akt and AMPK, and improves glucose and lipid metabolism. Next, we studied the role of vaspin on atherosclerosis. Vaspin inhibited arterial intimal thickening of balloon injured and cuff-injured vessels of rodent model. Vaspin binds to GRP78/VDAC complex on vascular endothelial cells and competes with the known VDAC ligand, kringle 5. Vaspin inhibits kringle 5-induced apoptosis pathway and enhances the phosphorylation of Akt. Subsequently, vaspin inhibits apoptosis of vascular endothelial cells.

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Vaspinと血管内皮細胞機能

2012

公益財団法人上原記念生命科学財団研究奨励金

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Authorship：Principal investigator

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Vaspinによる動脈硬化抑制とその作用機序の解明

2012

公益財団法人日本心臓財団日本心臓財団・アステラス・ファイザー「動脈硬化」Update研究助成

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Metabolic Syndrome and obesity （2024academic year） special - その他
Lecture: Metabolic Syndrome （2024academic year） special - その他
Practicals: Nephrology, Rheumatology, Endocrinology and Metabolism （2024academic year） special - その他
Research Projects: Nephrology, Rheumatology, Endocrinology and Metabolism （2024academic year） special - その他
Research and Practicals: Nephrology, Rheumatology, Endocrinology and Metabolism I （2024academic year） special - その他
Lecture and Research: Nephrology, Rheumatology, Endocrinology and Metabolism I （2024academic year） special - その他
Research and Practicals:Nephrology, Rheumatology, Endocrinology and Metabolism II （2024academic year） special - その他
Lecture and Research: Nephrology, Rheumatology, Endocrinology and Metabolism II （2024academic year） special - その他
Metabolic Syndrome and obesity （2023academic year） special - その他
Lecture: Metabolic Syndrome （2023academic year） special - その他
Practicals: Nephrology, Rheumatology, Endocrinology and Metabolism （2023academic year） special - その他
Research Projects: Nephrology, Rheumatology, Endocrinology and Metabolism （2023academic year） special - その他
Research and Practicals: Nephrology, Rheumatology, Endocrinology and Metabolism I （2023academic year） special - その他
Lecture and Research: Nephrology, Rheumatology, Endocrinology and Metabolism I （2023academic year） special - その他
Research and Practicals:Nephrology, Rheumatology, Endocrinology and Metabolism II （2023academic year） special - その他
Lecture and Research: Nephrology, Rheumatology, Endocrinology and Metabolism II （2023academic year） special - その他
Lecture: Metabolic Syndrome （2022academic year） special - その他
Research and Practicals: Nephrology, Rheumatology, Endocrinology and Metabolism I （2022academic year） special - その他
Lecture and Research: Nephrology, Rheumatology, Endocrinology and Metabolism I （2022academic year） special - その他
Research and Practicals:Nephrology, Rheumatology, Endocrinology and Metabolism II （2022academic year） special - その他
Lecture and Research: Nephrology, Rheumatology, Endocrinology and Metabolism II （2022academic year） special - その他
Lecture: Metabolic Syndrome （2021academic year） special - その他
Research Projects and Practicals: Medicine and Clinical Science I （2021academic year） special - その他
Research and Practicals: Nephrology, Rheumatology, Endocrinology and Metabolism I （2021academic year） special - その他
Research and Practicals: Nephrology, Rheumatology, Endocrinology and Metabolism I （2021academic year） special - その他
Lecture and Research Projects: Medicine and Clinical Science I （2021academic year） special - その他
Lecture and Research: Nephrology, Rheumatology, Endocrinology and Metabolism I （2021academic year） special - その他
Research Projects and Practicals: Medicine and Clinical Science II （2021academic year） special - その他
Lecture and Research Projects: Medicine and Clinical Science II （2021academic year） special - その他
Lecture and Research: Nephrology, Rheumatology, Endocrinology and Metabolism II （2021academic year） special - その他
Research Projects and Practicals: Medicine and Clinical Science I （2020academic year） special - その他
Research and Practicals: Nephrology, Rheumatology, Endocrinology and Metabolism I （2020academic year） special - その他
Lecture and Research Projects: Medicine and Clinical Science I （2020academic year） special - その他
Lecture and Research: Nephrology, Rheumatology, Endocrinology and Metabolism I （2020academic year） special - その他
Research Projects and Practicals: Medicine and Clinical Science II （2020academic year） special - その他
Research and Practicals:Nephrology, Rheumatology, Endocrinology and Metabolism II （2020academic year） special - その他
Lecture and Research Projects: Medicine and Clinical Science II （2020academic year） special - その他
Lecture and Research: Nephrology, Rheumatology, Endocrinology and Metabolism II （2020academic year） special - その他

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